Journal articles on the topic 'Lymphocyte'
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Chen, Lin-Ying, Julia Y. S. Tsang, Yun-Bi Ni, Siu-Ki Chan, Kui-Fat Chan, Sheng Zhang, and Gary M. Tse. "Lymphocyte subsets contribute to the degree of lobulitis and ductitis in sclerosing lymphocytic lobulitis of the breast." Journal of Clinical Pathology 69, no. 6 (November 18, 2015): 527–32. http://dx.doi.org/10.1136/jclinpath-2015-203334.
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AimsSclerosing lymphocytic lobulitis (SLL) of the breast is characterised by lymphocytic lobulitis, ductitis, vasculitis and dense keloidal fibrosis with epithelioid fibroblasts. However, the subsets of the infiltrating lymphocytes and their contribution to disease progression have not been fully explored.MethodsCD20, CD3, CD4, CD8 and regulatory T (Treg) lymphocytes were evaluated in the epithelial and vascular areas in SLL. The relationship between the lymphocyte subset in different regions and the degree of inflammation was analysed.ResultsLymphocytic infiltration was mainly located in peri-lobular, peri-ductal and peri-vascular areas. No significant differences between CD20 and CD3 lymphocytes were found in peri-epithelial areas. However, there were more intra-ductal/lobular epithelial CD3 than CD20 lymphocytes (p<0.001). For T lymphocyte subsets, more CD4 than CD8 lymphocytes were found in the peri-lobular/vascular regions (p≤0.026); but an opposite trend was seen in the intra-ductal/lobular regions (p<0.001). In the peri-lobular/vascular regions, generally, different lymphocyte subsets correlated with each other. Interestingly, in the peri-ductal region, only CD4 lymphocytes showed significant correlations with all other subsets (p≤0.020). Regarding their relationship with the degree of inflammation, significant positive correlations were observed for all subsets in peri-vascular/lobular regions (p≤0.045). Only regulatory T cells, but not the others, at the peri-ductal region showed significant correlation with the degree of inflammation at all three regions (p≤0.014).ConclusionsIn addition to B lymphocyte subsets, T lymphocyte subsets could be involved differently in SLL. CD4 lymphocytes may have a pivotal role in recruiting other subsets to the inflamed site, and triggered the cascade of inflammatory changes resulting in fibrosis.
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Winther, Birgit, Donald J. Innes, John Bratsch, and Frederick G. Hayden. "Lymphocyte Subsets in the Nasal Mucosa and Peripheral Blood during Experimental Rhinovirus Infection." American Journal of Rhinology 6, no. 4 (July 1992): 149–56. http://dx.doi.org/10.2500/105065892781874621.
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The local cellular response during rhinovirus infection was studied with immunohistochemical staining of lymphocyte subpopulations in the lamina propria of the nasal mucosa (inferior turbinate) in 25 biopsies from volunteers with experimental rhinovirus colds and compared with biopsies from healthy volunteers. Biopsies from rhinovirus infected volunteers, taken either in the early phase of the infection (days 3 and 5) or during convalescence (day 14) were evaluated in a semiquantitative fashion for degree of infiltration. Lymphocyte subpopulations also were counted on coded specimens. During experimental rhinovirus infection, no change could be observed in the overall degree of lymphocytic infiltration or in the numbers of T and B lymphocytes compared with control specimens. The overall degree of lymphocyte infiltration in the nasal mucosa was mild to moderate and consisted principally of T lymphocytes and only a few scattered B lymphocytes. Few natural killer lymphocytes were seen. These findings are similar to those in normal nasal mucosa and in contrast to the findings after topical application of recombinant interferon, which often results in a heavy lymphocyte infiltration. Lymphocyte subpopulation in the peripheral blood did not change when compared with prechallenge values in nine rhinovirus-infected volunteers.
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Park, Kenneth G. M., Steven D. Heys, Margaret A. McNurlan, Peter J. Garlick, and Oleg Eremin. "Lymphocyte Protein Synthesis In Vivo: a Measure of Activation." Clinical Science 86, no. 6 (June 1, 1994): 671–75. http://dx.doi.org/10.1042/cs0860671.
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1. The ‘flooding’ dose technique was used to measure rates of lymphocyte protein synthesis after infusion of [1-13C]leucine (20 atoms% enrichment, 4 g/70 kg body weight). Lymphocyte protein synthesis was measured in healthy subjects and in patients with metastatic colorectal cancer before and during infusion of recombinant interleukin-2. Rates of protein synthesis were compared with thymidine uptake in vitro and phenotypic analysis of lymphocytes. 2. The median rate of lymphocyte protein synthesis in four healthy subjects was 9% (range 7.2–11.4%/day) and in seven patients with colorectal cancer was 6.4% (range 4.2–8.2%/day). After recombinant interleukin-2 treatment the median rate of lymphocyte protein synthesis was 27.8% (range 25.2–33.7%/day). 3. The increased rates of lymphocyte protein synthesis in vivo, after recombinant interleukin-2 infusion, corresponded with increased rates of thymidine uptake and changes in the phenotypic expression of lymphocytes, but these were less consistent than the measured rates of protein synthesis. 4. It is concluded that lymphocyte activation is accompanied by a marked increase in lymphocytic protein synthesis which may have important implications for whole body protein metabolism. Furthermore, measurement of lymphocyte protein synthesis may provide a determination of lymphocyte activation in vivo.
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Choccalingam, Chidambharam. "Volume, conductance, and scatter parameters of neoplastic and nonneoplastic lymphocytes using Coulter LH780." Journal of Laboratory Physicians 10, no. 01 (January 2018): 085–88. http://dx.doi.org/10.4103/jlp.jlp_65_17.
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Abstract PURPOSE: Automated hematology analyzers yield a complete hematological profile including a complete blood count and a differential white blood cell count. The differential count is based on analyses of three parameters, namely, volume, conductance, and scatter (VCS). We aimed to evaluate the VCS parameters, histograms, and scatterplots of neoplastic and nonneoplastic lymphocytes. MATERIAL AND METHODS: Patients were grouped into four categories, namely, acute lymphoblastic leukemia (ALL), chronic systemic disorders, chronic lymphocytic leukemia (CLL), and acute viral disease. Lymphocytes from all four groups were compared with lymphocytes from normal participants. RESULTS AND CONCLUSIONS: The histogram for acute viral disease showed a trough at T1, which was slightly obliterated, and the F1 curve mildly extended to the right. The T1 for ALL was replaced with a peak at >40% of the preset limit. The F1 peak was shifted to left for CLL. The scatterplot for viral disease showed lymphocytes extending to the variant lymphocyte window. The lymphocytes of ALL extended to the blast window, with both increase in volume and mild increase in scatter. The lymphocytes in CLL were smaller and located below the normal lymphocyte region. Mean lymphocyte volume was significantly increased in ALL and was significantly decreased in CLL. Mean lymphocyte conductance was significantly increased in CLL and significantly decreased in both acute viral disease and ALL. Mean lymphocyte scatter was significantly decreased in acute viral disease and significantly increased in ALL.
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Schimpff, R. M., and A. M. Repellin. "In vitro effect of human growth hormone on lymphocyte transformation and lymphocyte growth factors secretion." Acta Endocrinologica 120, no. 6 (June 1989): 745–52. http://dx.doi.org/10.1530/acta.0.1200745.
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Abstract. Cultures of human blood peripheral lymphocytes were performed in the presence or absence of human growth hormone, and also of phytohemagglutinin and normal human serum 10%. After incubation for 48 h, the supernatants were tested for their ability to promote the uptake of [3H]thymidine into lectin-activated lymphocytes. Supernatants from lymphocyte-free control samples, treated in the same manner, were assayed under the same experimental conditions. Variance analysis of the different dose-response relationships was performed. The results of these in vitro experiments confirm that physiological levels of GH inhibit the lectin-induced lymphoproliferation and that lymphocytes secrete an 'activity' able to stimulate the incorporation of [3H]thymidine into lectin activated lymphocytes. Furthermore we show that: 1) Secretion of this lymphocyte-stimulating activity is increased by physiological levels of GH; 2) This lymphocytic secretion is not radioimmunoassayable IGF-I; 3) Using fast protein liquid chromatography (FPLC), this activity appears in fractions with various molecular weights.
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Li, Jianxu, Peng Guo, Masayuki Hirano, Brantley Herrin, and Max Cooper. "Cellular and molecular characterization of hagfish VLR-based adaptive immune system (VET2P.1043)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 207.15. http://dx.doi.org/10.4049/jimmunol.192.supp.207.15.
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Abstract Jawless vertebrates have an alternative adaptive immune system in which variable lymphocyte receptors (VLR) are somatically diversified through recombinatorial assembly of leucine-rich repeat cassettes during lymphocyte development. Three VLR loci (VLRA, VLRB, and VLRC) have been defined in lampreys and each is expressed by a distinct lymphocyte population. Lamprey VLRA and VLRC are expressed by T-like lineages of lymphocytes, whereas VLRB is expressed by a B-like lineage of lymphocytes, much like αβ T, γδ T and B cells in jawed vertebrates. Recently we have revised the nomenclature for the hagfish VLRs by defining a third VLR gene. Here, monoclonal and polyclonal antibodies were generated against invariant residues of hagfish VLRA, VLRB and VLRC and these were used to identify VLR-bearing lymphocytes and their products. We found that hagfish VLRA, VLRB and VLRC are expressed by three separate lymphocyte populations. Size-exclusion chromatography and western blot analysis indicated that multivalent VLRB proteins are released into the circulation, which suggests that hagfish VLRB+ cells are B-cell like. In contrast, neither VLRA nor VLRC was detectable in the plasma, supporting the hypothesis that these two lymphocyte populations are T-cell like. The demonstration of three lymphocyte populations in both lampreys and hagfish suggests that this tripartite lymphocytic differentiation program already existed in a common ancestor of the two cyclostome lineages around 480 Mya.
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Silverman, David A., and Dennis J. Chapron. "Lymphopenic Effect of Carbamazepine in a Patient with Chronic Lymphocytic Leukemia." Annals of Pharmacotherapy 29, no. 9 (September 1995): 865–67. http://dx.doi.org/10.1177/106002809502900906.
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Objective: To report a dramatic and reproducible suppressive effect of carbamazepine on circulating lymphocytes in an elderly woman with chronic lymphocytic leukemia. Case Summary: An elderly woman taking phenytoin for a stroke-associated seizure disorder had lymphocyte count of 28 800 × 106 cells/L. Speculating an unusual lymphadenopathic effect of the phenytoin therapy, carbamazepine therapy was substituted. After 15 weeks of carbamazepine treatment, the lymphocyte count declined to 3200 × 106 cells/L. Because of severe diarrhea, carbamazepine therapy was stopped and phenytoin therapy was reinstituted. At the end of 4 months of phenytoin treatment, the lymphocyte count had increased to 23 200 × 106 cells/L. Phenytoin therapy was discontinued and carbamazepine therapy was begun. The lymphocyte count decreased to 10 700 × 106 cells/L. Severe diarrhea recurred and phenytoin treatment was reinstituted. Over 12 days the lymphocyte count increased to 28 900 × 106 cells/L. Phenytoin therapy was stopped and valproic acid therapy was started. The lymphocyte count continued to increase during valproic acid therapy, reaching a peak of 114 300 × 106 cells/L. Discussion: In this patient with chronic lymphocytic leukemia, carbamazepine therapy had a significant and reproducible lymphopenic effect that was readily reversible upon discontinuation of the drug. Unfortunately, this effect was associated with severe diarrhea, preventing further attempts at exploiting this potentially beneficial action. Conclusions: Carbamazepine had a reproducible suppressive effect on lymphocyte counts in an elderly patient with chronic lymphocytic leukemia. This unique observation raises the possibility that carbamazepine therapy may have a useful effect in patients with chronic lymphocytic leukemia.
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Spain, B. A., D. M. Soliman, R. A. Sidner, and H. L. Twigg. "Enhanced proliferation and IL-2 secretion by lung lymphocytes from HIV-infected subjects." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 4 (October 1, 1995): L498—L506. http://dx.doi.org/10.1152/ajplung.1995.269.4.l498.
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Human immunodeficiency virus (HIV)-positive patients frequently develop a CD3+/CD8+ cytotoxic T cell lymphocytic alveolitis. This could occur through in situ expansion of lung lymphocytes. We evaluated lung and blood lymphocyte proliferation in asymptomatic HIV-infected individuals by measuring spontaneous and cytokine-induced tritiated thymidine incorporation. Interleukin (IL)-2 and IL-4 secretion was determined with the use of enzyme-linked immunosorbent assay, Western blotting, and immunoprecipitation techniques. Spontaneous proliferation by lung lymphocytes from HIV-positive patients was significantly greater than that of normal volunteers. Proliferation was confined to the CD8+ lymphocyte subset. Over time, spontaneous proliferation declined unless autologous alveolar macrophages (AM) were added, suggesting AM were providing additional stimulatory signals to lung lymphocytes. Lung and blood lymphocytes proliferated in response to IL-2 but not IL-4. Lymphocytes in HIV-infected lung spontaneously produced and secreted more IL-2 than either normal lung lymphocytes or autologous blood lymphocytes. IL-4 production was not detectable in either group. These findings support the hypothesis that lymphocytic alveolitis in asymptomatic HIV-positive patients results from IL-2-dependent in situ proliferation of CD3+/CD8+ cytotoxic T cells.
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Todorović, Jasna, Marko Dinčić, Jelena Nešović Ostojić, Ivan Zaletel, Srdjan Lopičić, Duško Dundjerović, Svetislav Tatić, et al. "Differences in Chromatin Texture and Nuclear Fractal Dimension Between Hashimoto's and Lymphocytic Thyroiditis Lymphocytes." Microscopy and Microanalysis 25, no. 3 (February 28, 2019): 762–68. http://dx.doi.org/10.1017/s1431927619000163.
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AbstractPrevious evidence suggested that lymphocytic thyroiditis (LT) was a variant of Hashimoto's thyroiditis (HT), thus the aim of the current study is to quantify structural changes in histological specimens taken from HT and LT patients. A total of 600 images containing a single lymphocyte nucleus (300 nuclei per group) were obtained from 20 patients with HT and LT. In order to quantify changes in the nuclear architecture of investigated lymphocytes, the fractal dimension (FD) and some gray-level co-occurrence matrix texture parameters (angular second moment, inverse difference moment, contrast, entropy, and correlation) were calculated for each nucleus. A statistically significant difference in the FD of the “binary-outlined” nucleus and that of the corresponding “black-and-white” nucleus was detected between HT and LT lymphocyte nuclei. In addition, there was also a statistically significant difference in contrast and correlation between HT and LT lymphocyte nuclei. In conclusion, the results of this study suggested that there was a difference in structural complexity between investigated lymphocyte nuclei; additionally, LT lymphocytes possessed probably more complex texture and larger variations as well as more asymmetrical nuclei compared with HT lymphocytes. Accordingly, these findings indicate that LT is probably not a variant of HT; however, more complex studies are necessary to estimate differences between these types of thyroiditis.
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Raje, Manoj, and Karvita B. Ahluwalia. "Motility of leukemic lymphocytes." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (August 12, 1990): 368–69. http://dx.doi.org/10.1017/s0424820100159382.
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In Acute Lymphocytic Leukemia motility of lymphocytes is associated with dissemination of malignancy and establishment of metastatic foci. Normal and leukemic lymphocytes in circulation reach solid tissues where due to in adequate perfusion some cells get trapped among tissue spaces. Although normal lymphocytes reenter into circulation leukemic lymphocytes are thought to remain entrapped owing to reduced mobility and form secondary metastasis. Cell surface, transmembrane interactions, cytoskeleton and level of cell differentiation are implicated in lymphocyte mobility. An attempt has been made to correlate ultrastructural information with quantitative data obtained by Laser Doppler Velocimetry (LDV). TEM of normal & leukemic lymphocytes revealed heterogeneity in cell populations ranging from well differentiated (Fig. 1) to poorly differentiated cells (Fig. 2). Unlike other cells, surface extensions in differentiated lymphocytes appear to originate by extrusion of large vesicles in to extra cellular space (Fig. 3). This results in persistent unevenness on lymphocyte surface which occurs due to a phenomenon different from that producing surface extensions in other cells.
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Wiley, J. S., J. R. Chen, G. P. Jamieson, and P. J. Thurlow. "Agonists for endothelial P2 purinoceptors trigger a signalling pathway producing Ca2+ responses in lymphocytes adherent to endothelial cells." Biochemical Journal 311, no. 2 (October 15, 1995): 589–94. http://dx.doi.org/10.1042/bj3110589.
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Recirculation of lymphocytes through the body involves their frequent adhesion to endothelial cells but little is known of the signalling pathways between these two cell types. Lymphocytes from patients with chronic lymphocytic leukaemia were loaded with the Ca(2+)-sensitive indicator, fura 2, and allowed to adhere to either glass or monolayers of human umbilical-vein endothelial cells. Addition of ATP or UTP (1-10 microM) to the superfusate produced a transient rise in cytosolic Ca2+ concentration in the lymphocytes adherent to endothelium (24 of 35 cells). In contrast, ATP or UTP (1-10 microM) had no effect on the cytosolic Ca2+ of lymphocytes attached to glass. As the only lymphocyte receptor for ATP (P2Z class) requires higher ATP concentrations (> 50 microM) for Ca2+ influx and is unresponsive to UTP, the involvement of a lymphocyte P2Z purinoceptor is unlikely. Various agonists including ATP, UTP, 2-methylthioATP, ADP and histamine all stimulated increases in endothelial cytosolic Ca2+ but only ATP and UTP (both agonists for endothelial P2U purinoceptors) triggered Ca2+ transients in adherent lymphocytes. Removal of extracellular Ca2+ did not abolish the ATP-induced rise in cytosolic Ca2+ concentration in lymphocytes adherent to endothelial cells. These findings show that stimulation of endothelial P2U purinoceptors triggers an endothelial-lymphocyte signalling pathway which releases internal Ca2+ in adherent lymphocytes.
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Li-Chang, Hector Hugo, Naziheh Assarzadegan, David Messenger, Andrea Grin, Christopher Howlett, and Richard Kirsch. "Correlation of peripheral blood lymphocyte counts with outcome and histopathologic features of lymphocytic inflammation in patients with stage II colorectal carcinoma." Journal of Clinical Oncology 32, no. 3_suppl (January 20, 2014): 475. http://dx.doi.org/10.1200/jco.2014.32.3_suppl.475.
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475 Background: The prognostic importance of the local antitumor immune response in colorectal carcinoma (CRC) is well established. Recent studies suggest that systemic antitumor immunity may also impact on survival. This study aimed to determine the relationship between peripheral blood lymphocyte counts (PBLCs), reactive features in regional lymph nodes, local tumoral/peri-tumoral lymphocytic inflammation and survival in stage II CRC. Methods: Resection specimens from 185 patients with stage II CRC were assessed for peri-tumoral lymphocytic inflammation, tumor-infiltrating lymphocytes, lymph node yield, lymph node size, and reactive changes in individual lymph nodes. Reactive changes were scored semi-quantitatively and given a reactivity [R] score of 1-4 based on the presence and size of germinal centers. Pre-operative PBLCs and neutrophil counts were recorded. Results: Lower peripheral lymphocyte counts were associated with advanced age (p = 0.016), T4 disease (p = 0.006), venous invasion (p = 0.006), lymph node yields <12 (p = 0.024), smaller mean nodal diameters (p = 0.021), absence of tumor-infiltrating lymphocytes (p = 0.002) and fewer highly-reactive lymph nodes (R score 4) per case (p = 0.032). Cox regression analysis revealed that advanced age (Hazard Ratio, 1.03 per year [95% confidence interval, 1.01-1.05]; p = 0.015) and higher peripheral lymphocyte counts (HR, 0.52 per 1x109cells/L [95% CI, 0.31-0.86]; p = 0.011) were independently predictive of disease-free survival. Neutrophil counts were not associated with outcome. A higher neutrophil to lymphocyte ratio was associated with worse survival on univariate, but not multivariable analysis. Conclusions: The PBLC is an independent predictor of survival in stage II CRC, and is significantly associated with the immune status of regional lymph nodes and the local lymphocytic immune response.
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Qiang, Wu, Lu Chunxiao, Wu Jiafeng, Li Xiaolong, Wang Fengxin, Gao Hong, and Liu Lei. "Association of T lymphocytes level and clinical severity in patients of COVID-19 in Shenzhen China." European Journal of Inflammation 19 (January 2021): 205873922110144. http://dx.doi.org/10.1177/20587392211014409.
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To explore the correlation between T lymphocytes and clinical severity in patients of COVID-19. A total of 183 COVID-19 patients were recruited in Shenzhen Third People’s Hospital from January 11 to February 16, 2020. According to the clinical classification criteria, they were divided into severe group (46 cases) and non-severe (137cases). T lymphocyte counts, lymphocyte subpopulation, IL-6 levels, and clinical outcomes were compared between the two groups. Compared with the non-severe group, the lymphocyte count, T lymphocyte count, T lymphocyte percentage, CD4+ T lymphocyte count, CD4+ T lymphocyte percentage, CD8+ T lymphocyte count, and CD8+ T lymphocyte percentage were lower in the severe group ( p < 0.05). Compared with the non-severe group, IL-6 were higher in the severe group ( p < 0.05). Compared with admission, the T lymphocyte count, CD4+ T lymphocyte count, and CD8+ T lymphocyte count were significantly increased upon discharge in severe patients, non-severe patients and all patients. Multivariate Logsitic regression analysis showed CD4+ T lymphocyte count (OR −0.011; 95% CI −0.041 to −0.001; p = 0.011), CD8+ T lymphocyte count (OR −0.14; 95% CI −0.048 to −0.003; p = 0.013) were closely correlated with the clinical severity in patients of COVID-19. Multivariate Logsitic regression analysis also showed CD4+ T lymphocyte count (OR −0.012; 95% CI −3.177 to 0.261; p = 0.021), CD8+ T lymphocyte count (OR −0.019; 95% CI −5.852 to 0.115; p = 0.004) were independent predictors of disease progressing to the composite endpoint. Subgroup analysis for critically ill patients: The T lymphocyte count, CD4+ T lymphocyte count, and CD8+ T lymphocyte count remained low in the death patients. The T lymphocyte count, CD4+ T lymphocyte count, and CD8+ T lymphocyte count recovered soon in the discharged patients. In the event of COVID-19 infection, the T-lymphoid system is the primary activated immune system. The T lymphocytes, CD4+ T lymphocytes, CD8+ T lymphocytes continued to be low may be significantly related to the deterioration of the disease, and may indicate a poor prognosis.
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Andrejsová, Lenka, Zuzana Šinkorová, Jiří Šinkora, Aleš Tichý, Alžběta Filipová, Markéta Němcová, and Marek Šinkora. "IN VIVO BIODOSIMETRY OF PORCINE T-LYMPHOCYTE SUBSETS AND NK CELLS." Radiation Protection Dosimetry 186, no. 2-3 (December 2019): 181–85. http://dx.doi.org/10.1093/rpd/ncz199.
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Abstract The aim of the present study was to evaluate the biodosimetric potential of peripheral blood lymphocytes, particularly of T-cell subsets (null and T helper) and natural killer cells (NK), upon exposure to gamma irradiation (60Co) in vivo. For this purpose, the change in relative numbers of NK cells and T-lymphocyte subsets, as well as in the H2AX phosphorylation rate, were evaluated as potential early markers of the lymphocytic response to irradiation in vivo. These experiments were performed on a Large White Pig model. As a result, significant but not dose-dependent changes in the proportion of lymphocyte subpopulations (NK cells, null and T helper cells) were found after exposure to ionising radiation in vivo. On the other hand, circulating NK cells showed relatively higher radioresistance capacity when compared to the T-lymphocyte subsets; however, gamma-H2AX expression showed no significant difference between the evaluated lymphocyte subsets.
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Yang, Jiale, Xiaojian Zhu, and Jun Feng. "The Changes in the Quantity of Lymphocyte Subpopulations during the Process of Sepsis." International Journal of Molecular Sciences 25, no. 3 (February 5, 2024): 1902. http://dx.doi.org/10.3390/ijms25031902.
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Sepsis remains a global challenge, especially in low- and middle-income countries, where there is an urgent need for easily accessible and cost-effective biomarkers to predict the occurrence and prognosis of sepsis. Lymphocyte counts are easy to measure clinically, and a large body of animal and clinical research has shown that lymphocyte counts are closely related to the incidence and prognosis of sepsis. This review extensively collected experimental articles related to lymphocyte counts since the unification of the definition of sepsis. The article categorizes and discusses the relationship between absolute lymphocyte counts, intrinsic lymphocyte subsets, effector T-lymphocytes, B-lymphocytes, dendritic cells, and the incidence and prognosis of sepsis. The results indicate that comparisons of absolute lymphocyte counts alone are meaningless. However, in addition to absolute lymphocyte counts, innate lymphocyte subsets, effector T-cells, B-lymphocytes, and dendritic cells have shown certain research value in related studies.
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Milicevic, Novica. "T lymphocytes are necessary for the peripheral phase of B lymphocyte maturation." Srpski arhiv za celokupno lekarstvo 136, Suppl. 2 (2008): 166–70. http://dx.doi.org/10.2298/sarh08s2166m.
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Until recently, B lymphocyte maturation was considered to be independent of the thymus and T lymphocytes. However, using nude animals, which lack the functional thymus, we have shown that T lymphocytes are required for the peripheral phase of B lymphocyte maturation. We showed that the proportion of immature B lymphocyte subsets (CD90highIgMhigh and CD90highIgMlow) was significantly increased, whereas that of mature B lymphocyte subsets (CD90?IgMlow and CD90?IgMhigh) was decreased in the peripheral blood and lymph nodes of nude rats. In addition, the expression of functionally important surface molecules MHC class II, ICAM-1, CD44 and L-selectin was significantly down-regulated both on immature and mature B lymphocyte subsets. The implantation of thymic tissue under the kidney capsule of nude rats alleviated the block in B lymphocyte maturation and normalized of the defective expression of surface molecules. Comparable effects were seen after the adoptive transfer of T lymphocytes. This shows that in nude rats B lymphocytes do not mature properly due to the lack of T cell help and that T lymphocytes are required for the peripheral phase of B lymphocyte maturation, as well as for the appropriate expression of surface molecules. This should be considered when treating patients with T lymphocyte deficiencies.
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Jalkanen, ST, and EC Butcher. "In vitro analysis of the homing properties of human lymphocytes: developmental regulation of functional receptors for high endothelial venules." Blood 66, no. 3 (September 1, 1985): 577–82. http://dx.doi.org/10.1182/blood.v66.3.577.577.
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Abstract Circulating lymphocytes leave the blood by binding to specialized high endothelial cells lining postcapillary venules in lymphoid organs or sites of chronic inflammations, migrating through the vessel wall into the surrounding tissue. The capacity of lymphocytes to recognize and bind to high endothelial venules (HEVs) is thus central to the overall process of lymphocyte traffic and recirculation. We show that viable human lymphocytes bind selectively to HEVs in frozen sections of normal human lymph nodes, thus defining a simple in vitro model for the study of human lymphocyte homing properties. Optimal conditions for the quantitative analysis of lymphocyte-HEV interaction are described. Furthermore, by using this assay, we demonstrate that the ability of human lymphocyte populations to bind to HEVs parallels their presumed migratory status in vivo. Thus, thymocytes and bone marrow cells, which are sessile in vivo, bind poorly to HEVs in comparison with mature circulating lymphocytes in peripheral blood or in peripheral lymphoid tissues. These results indicate that HEV-binding ability is a regulated property of mature lymphocytes and, as demonstrated previously in animal models, probably plays a fundamental role in controlling lymphocyte traffic in humans. The in vitro model of lymphocyte-HEV interaction thus provides a unique means to assay the migratory properties of normal and neoplastic human lymphocyte subsets, to analyze the role of lymphocyte traffic mechanisms in normal and pathologic inflammatory reactions, and to define some of the molecular mechanisms responsible for the control of lymphocyte migration and positioning in humans.
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Jalkanen, ST, and EC Butcher. "In vitro analysis of the homing properties of human lymphocytes: developmental regulation of functional receptors for high endothelial venules." Blood 66, no. 3 (September 1, 1985): 577–82. http://dx.doi.org/10.1182/blood.v66.3.577.bloodjournal663577.
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Circulating lymphocytes leave the blood by binding to specialized high endothelial cells lining postcapillary venules in lymphoid organs or sites of chronic inflammations, migrating through the vessel wall into the surrounding tissue. The capacity of lymphocytes to recognize and bind to high endothelial venules (HEVs) is thus central to the overall process of lymphocyte traffic and recirculation. We show that viable human lymphocytes bind selectively to HEVs in frozen sections of normal human lymph nodes, thus defining a simple in vitro model for the study of human lymphocyte homing properties. Optimal conditions for the quantitative analysis of lymphocyte-HEV interaction are described. Furthermore, by using this assay, we demonstrate that the ability of human lymphocyte populations to bind to HEVs parallels their presumed migratory status in vivo. Thus, thymocytes and bone marrow cells, which are sessile in vivo, bind poorly to HEVs in comparison with mature circulating lymphocytes in peripheral blood or in peripheral lymphoid tissues. These results indicate that HEV-binding ability is a regulated property of mature lymphocytes and, as demonstrated previously in animal models, probably plays a fundamental role in controlling lymphocyte traffic in humans. The in vitro model of lymphocyte-HEV interaction thus provides a unique means to assay the migratory properties of normal and neoplastic human lymphocyte subsets, to analyze the role of lymphocyte traffic mechanisms in normal and pathologic inflammatory reactions, and to define some of the molecular mechanisms responsible for the control of lymphocyte migration and positioning in humans.
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Nakai, Akiko, Yuki Hayano, Fumika Furuta, Masaki Noda, and Kazuhiro Suzuki. "Control of lymphocyte egress from lymph nodes through β2-adrenergic receptors." Journal of Experimental Medicine 211, no. 13 (November 24, 2014): 2583–98. http://dx.doi.org/10.1084/jem.20141132.
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Lymphocyte recirculation through secondary lymphoid organs is essential for immunosurveillance and lymphocyte effector functions. Here, we show that signals through β2-adrenergic receptors (β2ARs) expressed on lymphocytes are involved in the control of lymphocyte dynamics by altering the responsiveness of chemoattractant receptors. Agonist stimulation of lymphocyte β2ARs inhibited egress of lymphocytes from lymph nodes (LNs) and rapidly produced lymphopenia in mice. Physiological inputs from adrenergic nerves contributed to retention of lymphocytes within LNs and homeostasis of their distribution among lymphoid tissues. β2ARs physically interacted with CCR7 and CXCR4, chemokine receptors promoting lymphocyte retention in LNs. Activation of β2ARs enhanced retention-promoting signals through CCR7 and CXCR4, and consequently inhibited lymphocyte egress from LNs. In models of T cell–mediated inflammatory diseases, β2AR-mediated signals inhibited LN egress of antigen-primed T cells and reduced their recruitment into peripheral tissues. Thus, this study reveals a novel mechanism for controlling lymphocyte trafficking and provides additional insights into immune regulation by the nervous system.
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Klein, Ami, Michael Lishner, Barbara Bruser, John E. Curtis, Dominick J. Amato, and Aaron Malkin. "Cortisol catabolism by lymphocytes of patients with chronic lymphocytic leukemia." Biochemistry and Cell Biology 68, no. 4 (April 1, 1990): 810–13. http://dx.doi.org/10.1139/o90-118.
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A low rate of catabolism of cortisol by lymphocytes correlates with high sensitivity of the cells to the steroid and causes them to die at a greater rate than control samples. Since lymphocytes of patients with chronic lymphocytic leukemia respond to treatment with glucocorticosteroids and are cortisol sensitive, we attempted to see whether their capability to catabolize cortisol differs from that of normal lymphocytes. No difference was found between the two groups of cells with regard to the pattern of cortisol metabolites. However, the lymphocytes of the chronic lymphocytic leukemia groups showed a total cortisol catabolism per cell that was significantly lower than that of the control group. Patients with low lymphocyte count in peripheral blood showed a relatively higher cortisol metabolism by lymphocytes per cell than those with high counts.Key words: lymphocytes, cortisol, catabolism, chronic lymphocytic leukemia, morbidity.
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Yakovlev, P. G., and D. A. Klyushin. "Lymphocytes in peripheral blood as differential indicator of the stage of pathological condition in urooncological patients." Likarska sprava, no. 8 (December 30, 2017): 83–89. http://dx.doi.org/10.31640/ls-2017-8-11.
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Absolute lymphocyte count and neutrophil/lymphocyte ratio are the indicators of systemic inflammatory response involved in pathogenesis and progression of cancer. We demonstrate that absolute lymphocyte count and share of lymphocytes in peripheral blood truly differentiate between different states of the disease: urological cancer, healthy individual, benign urological condition and urological cancer after radical treatment. Considering involvement of lymphocytes in systemic inflammatory response and pathogenesis of cancer medical interventions targeting lymphocyte may yield therapeutic benefits.
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Wu, N. W., S. Jalkanen, P. R. Streeter, and E. C. Butcher. "Evolutionary conservation of tissue-specific lymphocyte-endothelial cell recognition mechanisms involved in lymphocyte homing." Journal of Cell Biology 107, no. 5 (November 1, 1988): 1845–51. http://dx.doi.org/10.1083/jcb.107.5.1845.
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Tissue-specific interactions with specialized high endothelial venules (HEV) direct the homing of lymphocytes from the blood into peripheral lymph nodes, mucosal lymphoid organs, and tissue sites of chronic inflammation. These interactions have been demonstrated in all mammalian species examined and thus appear highly conserved. To assess the degree of evolutionary divergence in lymphocyte-HEV recognition mechanisms, we have studied the ability of lymphocytes to interact with HEV across species barriers. By using an in vitro assay of lymphocyte binding to HEV in frozen sections of lymphoid tissues, we confirm that mouse, guinea pig, and human lymphocytes bind to xenogeneic as well as homologous HEV. In addition, we show that mouse and human lymphoid cell lines that bind selectively to either peripheral lymph node or mucosal vessels (Peyer's patches, appendix) in homologous lymphoid tissues exhibit the same organ specificity in binding to xenogeneic HEV. Furthermore, monoclonal antibodies that recognize lymphocyte "homing receptors" and block homologous lymphocyte binding to peripheral lymph node or to mucosal HEV, also inhibit lymphocyte interactions with xenogeneic HEV in a tissue-specific fashion. Similarly, anti-HEV antibodies against organ-specific mouse high endothelial cell "addressins" involved in lymphocyte homing to peripheral lymph node or mucosal lymphoid organs, not only block the adhesion of mouse lymphocytes but also of human lymphocytes to target mouse HEV. The results illustrate a remarkable degree of functional conservation of elements mediating these cell-cell recognition events involved in organ-specific lymphocyte homing.
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Forsyth, Christopher B., and Herbert L. Mathews. "Lymphocyte Adhesion to Candida albicans." Infection and Immunity 70, no. 2 (February 2002): 517–27. http://dx.doi.org/10.1128/iai.70.2.517-527.2002.
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ABSTRACT Adherence of lymphocytes to the fungus is the first step in the direct lymphocyte-mediated antifungal effect against Candida albicans. In this study we identified macrophage-1 antigen (Mac-1) (CD11b/CD18, αM/β2) as the lymphocyte surface structure responsible for the adhesion of activated lymphocytes to the hyphal form of the fungus. Antibodies specific for epitopes of the α-subunit (CD11b) and the β2-subunit (CD18) of Mac-1 were shown to completely eliminate lymphocyte adhesion to C. albicans hyphae. Lymphocyte adhesion to C. albicans was also inhibited significantly by known ligands of Mac-1, including the extracellular matrix proteins laminin and fibrinogen, as well as engineered peptides containing arginine-glycine-aspartic acid sequences and the disintegrin echistatin. N-Acetyl-d-glucosamine and β-glucan, which inhibit Mac-1-mediated adhesion to the yeast, blocked lymphocyte adhesion to hyphae. NIH 3T3 fibroblast transfectants expressing human CD11b/CD18 bound to C. albicans, and their binding was inhibited by antibodies specific for CD11b/CD18. Finally, antibodies specific for CD11b/CD18 effectively inhibited the capacity of activated lymphocytes to have an antifungal effect against hyphae. Our results clearly identify Mac-1 (CD11b/CD18) as the lymphocyte surface structure that mediates activated lymphocyte adhesion to C. albicans and the resultant antifungal effect of the lymphocytes.
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Carrara, C. B., M. Ferrante, and G. L. Zapata. "Nodular lymphocytic conjunctivitis in a horse - case report." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 75, no. 1 (2023): 113–16. http://dx.doi.org/10.1590/1678-4162-12838.
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ABSTRACT The case of an equine with nodular lymphocytic conjunctivitis is described. A 14-year-old crossbred mare was seen presenting with development of a mass in the nasal angle of the right eye, behind the third eyelid. The tutor reported slow growth over 4 years, always accompanied by epiphora, and that no treatment had been performed prior to consultation. The histopathological and immunohistochemical results found a nodular, subepithelial structure, composed predominantly of densely packed small lymphocytes. Through the exams, associated with studies with monoclonal anti B lymphocyte antibodies and polyclonal anti T lymphocyte antibodies, the diagnosis of nodular lymphocytic conjunctivitis was reached. Only clinical pharmacological treatment was chosen, based on the use of topical and intralesional hydrocortisone acetate. After one month of treatment the mass completely disappeared without sequelae.
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Majstoravich, Sonja, Jinyi Zhang, Susan Nicholson-Dykstra, Stefan Linder, Wilhelm Friedrich, Katherine A. Siminovitch, and Henry N. Higgs. "Lymphocyte microvilli are dynamic, actin-dependent structures that do not require Wiskott-Aldrich syndrome protein (WASp) for their morphology." Blood 104, no. 5 (September 1, 2004): 1396–403. http://dx.doi.org/10.1182/blood-2004-02-0437.
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Abstract Short microvilli cover the surfaces of circulating mammalian lymphocytes. The surfaces of monocytes and neutrophils are very different, containing ruffles as their predominant structure. In this study, we present the first quantitative characterization of lymphocyte microvilli. From analysis of scanning electron micrographs, we find that median microvillar length and surface density range from 0.3 to 0.4 μm and 2 to 4 microvilli/μm2, respectively, on lymphocytes from a variety of sources. As with similar structures from other cells, lymphocyte microvilli contain parallel bundles of actin filaments. Lymphocyte microvilli rapidly disassemble when exposed to the actin-sequestering molecule, Latrunculin A. This disassembly parallels cellular actin filament depolymerization and is complete within 2 minutes, suggesting that lymphocyte microvilli undergo continuous assembly and disassembly. In contrast to previous reports suggesting lymphocyte microvillar density to be reduced on lymphocytes from Wiskott-Aldrich syndrome (WAS) patient, we find no such deficiency in either mouse or human WAS protein (WASp)–deficient lymphocytes. These results suggest that WASp is either not involved in or is redundant in the rapid dynamics of lymphocyte microvilli.
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Zhang, Qiao-quan, Yan-fang Zhang, Nian Yu, Xing-jian Lin, and Qing Di. "Differential Diagnosis of Autoimmune Encephalitis from Infectious Lymphocytic Encephalitis by Analysing the Lymphocyte Subsets of Cerebrospinal Fluid." Analytical Cellular Pathology 2019 (December 3, 2019): 1–6. http://dx.doi.org/10.1155/2019/9684175.
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This study is aimed at investigating the lymphocyte subsets of cerebrospinal fluid (CSF) to provide possible differential diagnostic values and better understand the pathophysiological mechanism underlying autoimmune encephalitis (AE) and infectious lymphocytic encephalitis. A series of CD markers, including CD3/4/8/20 representing different types and developmental stages of lymphocytes, were used to count the corresponding subpopulations of CSF from clinical and laboratory confirmed cases of anti-N-methyl-D-aspartate receptor AE (NMDAR-AE), herpes simplex virus encephalitis (HSVE), and tuberculous meningitis (TBM). The percentages of lymphocytes observed and the CD4 : CD8 ratios were compared between the three groups. There were no significant differences of the percentage of total lymphocytes, CD3 cells, and CD4 cells of CSF among each group. However, there were strongly statistical differences of the CD4 : CD8 ratio in CSF of each group with 0.6 : 1 in NMDAR-AE, 0.9 : 1 in HSVE, and 3.2 : 1 in TBM. The percentage of CD20 B lymphocytes in NMDAR-AE was statistically higher than that of other groups. The distinct percentages of lymphocyte subpopulations of CSF appeared to be characteristic and could potentially serve as diagnostic indicators. Further verification and research will be necessary to clarify the significance and nature of CD4 : CD8 ratios and B lymphocytes in CSF between AE and the infectious lymphocytic encephalitis.
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Peng, Cong, Zongwei Guo, Yue Zhao, Rui Li, Liang Wang, and Wenping Gong. "Effect of Lymphocyte Subsets on Bone Density in Senile Osteoporosis: A Retrospective Study." Journal of Immunology Research 2022 (October 26, 2022): 1–11. http://dx.doi.org/10.1155/2022/3337622.
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Background. Several studies have shown that lymphocyte subsets can mediate the occurrence of osteoporosis (OP); however, the predictive ability of lymphocyte subsets in senile OP has not been elucidated. Purpose. To investigate the ability of lymphocyte subsets to predict senile osteoporosis (OP). Methods and Materials. This study included 44 patients with senile OP and 44 without OP. Dual-energy X-ray absorptiometry (DEXA) was used to determine bone mineral density (BMD). Flow cytometry was used to analyze the absolute counts of the lymphocyte subsets and cytokine levels. Finally, the correlation between BMD and lymphocyte subset counts in the two groups was analyzed. Results. There were no significant differences in age, sex, or weight between the OP and non-OP groups. The absolute counts of total T lymphocytes and CD8+ T lymphocytes in the OP group were significantly lower than those in the non-OP group. The levels of IFN-γ or TNF-α in the OP group were significantly higher or lower, respectively, than those in the non-OP group. PCA showed that age, BMI, total T lymphocytes, CD4+ T lymphocytes, CD8+ T lymphocytes, and B lymphocytes were the principal components of senile OP. The linear regression equation showed that BMD of the right femoral neck significantly decreased with a decline in CD8+ T lymphocyte counts. Conclusion. BMD decreased with a decrease in CD8+ T lymphocytes. The mechanism by which lower lymphocyte subsets lead to lower BMD may be related to abnormal bone metabolism caused by immune aging. Therefore, we considered that CD8+ T lymphocytes could be used to predict the incidence of senile OP.
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Zhang, Jimin, Satish Devadas, and Yufang Shi. "Differential roles of CD95L and TRAIL in activation-induced cell death of cytotoxic T lymphocytes (110.22)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 110.22. http://dx.doi.org/10.4049/jimmunol.188.supp.110.22.
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Abstract Cytotoxic T lymphocytes can be differentiated into type 1 (Tc1) and type 2 (Tc2) subsets as their T helper counterparts. Interestingly, our investigation in activation-induced cell death mechanisms reveals that CD95L mediates cell death in Tc1 lymphocytes and that Tc2 lymphocytes require TRAIL. Cell death in both subsets is also dependent on caspases. Inhibiting CD95L binding to its receptors in Tc1 lymphocytes from wild type mice displays altered Tc1 lymphocyte death, while Inhibiting TRAIL binding to its receptors in Tc2 lymphocytes shows altered Tc2 lymphocyte death. Activation-induced cell death in both Tc1 and Tc2 lymphocyte subsets can be blocked by pan caspase inhibitors. Moreover, Tc2 lymphocytes differentiated from TRAIL knockout mice show alleviated cell death. Rescued Tc2 lymphocytes secrete significantly higher amounts of IL-4, IL-5 and IL-10 while Tc1 lymphocytes produce higher IFN-γ and TNF-α. Our results indicate that CD95L and TRAIL play differential seminal roles in activation-induced cell death of these two cytotoxic T lymphocyte subsets, and that their different sensitivity to activation-induced cell death can alter CD8+ phenotype. With our study we conclude that Tc1 lymphocyte activation-induced cell death is mediated by CD95L while Tc2 lymphocytes undergo TRAIL-dependent activation-induced cell death.
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Li, Lijin, Sharon M. Dial, Monika Schmelz, Margaret A. Rennels, and Neil M. Ampel. "Cellular Immune Suppressor Activity Resides in Lymphocyte Cell Clusters Adjacent to Granulomata in Human Coccidioidomycosis." Infection and Immunity 73, no. 7 (July 2005): 3923–28. http://dx.doi.org/10.1128/iai.73.7.3923-3928.2005.
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ABSTRACT The in situ immunologic response in human coccidioidomycosis remains undefined. To explore this further, pulmonary necrotizing coccidioidal granulomata were examined using immunohistochemical staining for lymphocyte subsets and for the cytokines interleukin-10 (IL-10) and gamma interferon (IFN-γ). Discrete perigranulomatous lymphocytic clusters were seen in eight of nine tissues examined. In these tissues, T lymphocytes (CD3+) significantly outnumbered B lymphocytes (CD20+) in the mantle area of the granulomata (P = 0.028), whereas the clusters were composed of roughly equal numbers of T and B lymphocytes. While the number of cells in the mantle expressing IL-10 was similar to those in the perigranulomatous clusters, there were significantly more cells expressing IFN-γ in the mantle than in the clusters (P = 0.037). Confocal microscopy revealed that CD4+ T lymphocytes and B lymphocytes are associated with IL-10 production. CD4+CD25+ T lymphocytes were identified in the perigranulomatous clusters but were not associated with IL-10 production. This is the first report noting perigranulomatous lymphocyte clusters and IL-10 in association with human coccidioidal granulomata and suggests that down-regulation of the cellular immune response is occurring within coccidioidal granulomata.
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Van Steensel, Maurice A. M., Michel Van Gelder, Ariënne M. W. Van Marion, Bernd Kremer, and Jorge Frank. "T-cell Large Granular Lymphocytic Leukaemia with an Uncommon Clinical and Immunological Phenotype." Acta Dermato-Venereologica 89, no. 2 (December 10, 2008): 172–74. http://dx.doi.org/10.2340/00015555-0589.
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A 39-year-old man presented with a rapidly growing unilateral painless nodule on the right cheek. Histopathological examination and peripheral blood analysis both showed a population of T-cell large granular lymphocytes, which were CD1+, CD2+, CD5+, CD7+ and CD16+, with expression of cutaneous lymphocyte-associated antigen. Further laboratory examination revealed severe neutropaenia, relative lymphocytosis and a clonally rearranged T-cell receptor. The cutaneous manifestation of T-cell large granular lymphocytic leukaemia is very rare. In this particular patient, however, it was instrumental in establishing the diagnosis and may have been enabled by the expression of cutaneous lymphocyte-associated antigen on the cell surface.
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Silber, R., CM Farber, E. Papadopoulos, D. Nevrla, L. Liebes, M. Bruck, R. Brown, and ZN Canellakis. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (October 15, 1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.2038.
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Abstract Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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Silber, R., CM Farber, E. Papadopoulos, D. Nevrla, L. Liebes, M. Bruck, R. Brown, and ZN Canellakis. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (October 15, 1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.bloodjournal8082038.
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Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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Nishiyama-Naruke, Anita, and Rui Curi. "Phosphatidylcholine participates in the interaction between macrophages and lymphocytes." American Journal of Physiology-Cell Physiology 278, no. 3 (March 1, 2000): C554—C560. http://dx.doi.org/10.1152/ajpcell.2000.278.3.c554.
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The role of phosphatidylcholine molecules as mediator for the control of lymphocyte proliferation by macrophages was investigated. Phosphatidylcholine added to the culture medium inhibited the concanavalin A-stimulated lymphocyte proliferation in a concentration-dependent manner. The potency of this effect was dependent on the presence of arachidonic acid in the phosphatidylcholine molecules. The phosphatidylcholine transfer from macrophages to lymphocytes was then investigated. Macrophages incorporated phosphatidylcholine at a much higher rate than lymphocytes and exported phosphatidylcholine to the culture medium. When cocultured, a significant amount of phosphatidylcholine incorporated by macrophages was transferred to lymphocytes. To examine the possible physiological importance of the transfer process, the lymphocyte proliferation was measured in coculture conditions. Macrophages were treated with phosphatidylcholine and washed, and then these cells were cocultured with concanavalin A-stimulated lymphocytes. The effect observed in coculture was an inhibition of lymphocyte proliferation, which was also dependent on the molecular species of the phosphatidylcholine. Therefore, phosphatidylcholine may act as a mediator of the macrophage effect on lymphocyte proliferation.
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Steeber, D. A., N. E. Green, S. Sato, and T. F. Tedder. "Lyphocyte migration in L-selectin-deficient mice. Altered subset migration and aging of the immune system." Journal of Immunology 157, no. 3 (August 1, 1996): 1096–106. http://dx.doi.org/10.4049/jimmunol.157.3.1096.
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Abstract Lymphocyte trafficking across high endothelial venules (HEV) of peripheral lymph nodes (PLN) is dependent upon lymphocyte expression of L-selectin. Mice that lack this adhesion molecule provide an opportunity to determine the long-term role of L-selectin-mediated migration in the maintenance of leukocyte subpopulations. HEV in L-selectin-deficient mice were phenotypically, morphologically, and functionally comparable with wild-type mice, although there was a 70 to 90% reduction in the number of lymphocytes within PLN. These lymphocytes most likely entered PLN through the afferent lymphatics, since they did not migrate into PLN of normal mice during short-term homing experiments. The impaired trafficking of lymphocytes across PLN-HEV resulted in the accumulation of memory (CD18highCD44high) lymphocytes within PLN, and also altered the distribution of lymphocyte subpopulations within other tissues. Specifically, a 30 to 55% increase in splenic cellularity occurred due to increases in both naive and memory lymphocytes. Circulating lymphocyte numbers or subpopulations were not altered in young L-selectin-deficient mice, but circulating monocyte numbers were increased nearly threefold. In contrast, older L-selectin-deficient mice had disproportionate increases of both naive and memory CD4+ T cells present within spleen and blood. These results and the finding that memory lymphocytes in wild-type mice expressed L-selectin demonstrate a requirement for L-selectin in the regulation of memory lymphocyte migration. Therefore, L-selectin-dependent pathways of lymphocyte migration are important for the normal migration of both naive and memory lymphocytes.
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Colson, Y. L., B. H. Markus, A. Zeevi, and R. J. Duquesnoy. "Increased lymphocyte adherence to human arterial endothelial cell monolayers in the context of allorecognition." Journal of Immunology 144, no. 8 (April 15, 1990): 2975–84. http://dx.doi.org/10.4049/jimmunol.144.8.2975.
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Abstract The interactions of alloreactive T lymphocytes with the vascular endothelium were studied in an in vitro model of lymphocyte adherence to cultured human arterial endothelial cell (HAEC) monolayers. Donor-primed lymphocytes (DPL) were shown to have significantly greater adherence to donor HAEC than were third-party primed lymphocytes. Limiting dilution analysis of adherent DPL showed an enrichment of donor-reactive lymphocytes compared with nonadherent DPL. This study examines the allospecific nature of this increased lymphocyte adherence. HAEC constitutively express class I HLA Ag and can be induced by IFN-gamma to express class II Ag. DPL adherence to class I+ HAEC was inhibited only in the presence of mAb directed against class I Ag. DPL adherence to class I+ and class II+ HAEC was inhibited in the presence of mAb directed against class I and class II Ag. Class I- and class II-specific adherence was also shown to involve CD8 and CD4 molecules, respectively, whereas lymphocyte function-associated Ag do not appear to play a major role in long term alloreactive lymphocyte adherence to HAEC. These findings suggest that alloreactive lymphocyte adherence to HAEC is mediated by two mechanisms. One is based on allorecognition, primarily of HLA Ag, and the other is related to presumably non-Ag-specific interactions between activated lymphocytes and the vascular endothelium. The studies presented provide evidence to suggest that HLA-specific lymphocyte adherence to endothelium may significantly contribute to the development of alloreactive lymphocyte infiltrates within the allograft.
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West, Charles A., Chufa He, Mei Su, Timothy W. Secomb, Moritz A. Konerding, Alan J. Young, and Steven J. Mentzer. "Focal topographic changes in inflammatory microcirculation associated with lymphocyte slowing and transmigration." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 4 (October 1, 2001): H1742—H1750. http://dx.doi.org/10.1152/ajpheart.2001.281.4.h1742.
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Microcirculation is the primary mechanism for delivering lymphocytes to inflammatory tissues. Blood flow within microvessels ensures a supply of lymphocytes at the blood-endothelial interface. Whether the structure of the inflammatory microcirculation facilitates lymphocyte transmigration is less clear. To illuminate the microcirculatory changes associated with lymphocyte transmigration, we used intravital videomicroscopy to examine the dermal microcirculation after application of the epicutaneous antigen oxazolone. Intravascular injection of fluorescein-labeled dextran demonstrated focal topographic changes in the microcirculation. These focal changes had the appearance of loops or hairpin turns in the oxazolone-stimulated skin. Changes were maximal at 96 h and coincided with peak lymphocyte recruitment. To determine whether these changes were associated with lymphocyte transmigration, lymphocytes obtained from efferent lymph of draining lymph nodes at 96 h were fluorescently labeled and reinjected into inflammatory microcirculation. Epifuorescence intravital video microscopy demonstrated focal areas were associated with lymphocyte slowing and occasional transmigration. In contrast, focal loops and lymphocyte slowing were rarely observed in the contralateral control microcirculation. Results suggest that structural adaptations in inflammatory microcirculation represented by focal topographic changes may contribute to regulation of tissue entry by recirculating lymphocytes.
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Hay, John B., and William N. Andrade. "Lymphocyte recirculation, exercise, and immune responses." Canadian Journal of Physiology and Pharmacology 76, no. 5 (May 1, 1998): 490–96. http://dx.doi.org/10.1139/y98-051.
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Alterations in leukocyte concentrations in the blood are associated with exercise, stress, and other pathophysiological perturbations. The continuous migration and redistribution of cells of the recirculating lymphocyte pool between the blood and lymphatic systems can be influenced by a variety of physiological, immunological, and pathological processes. The phenotypic distribution of lymphocyte subsets is not the same in blood, afferent lymph, and efferent lymph, and cell-tracking experiments have shown that lymphocytes vary in their migratory properties. The most comprehensive physiological studies tracking these cells in vivo have been done in sheep. It has been shown that lymph-derived cells have different migratory capacities than blood-derived lymphocytes, that antigenic challenge of a single lymph node can first reduce the output of lymphocytes from the node and then markedly increase the recruitment from the blood and subsequently the output into efferent lymph. In most mammals, the blood pool of lymphocytes represents only about 1% of the total lymphocytes and only a small fraction of the recirculating lymphocyte pool. Therefore, testing the effects of exercise on lymphocyte recirculation by examining blood samples only requires considerable deduction and inference to interpret multicompartmental effects.Key words: lymphocyte migration, blood, lymph, lymph nodes.
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Park, Suk W., Walter Royal, Richard D. Semba, Gordon W. Wiegand, and Diane E. Griffin. "Expression of Adhesion Molecules and CD28 on T Lymphocytes during Human Immunodeficiency Virus Infection." Clinical Diagnostic Laboratory Immunology 5, no. 4 (July 1, 1998): 583–87. http://dx.doi.org/10.1128/cdli.5.4.583-587.1998.
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ABSTRACT Adhesion molecules, which play a major role in lymphocyte circulation, have not been well characterized in human immunodeficiency virus (HIV) infection. T-lymphocyte populations, including CD3, CD4, CD28, and adhesion molecules (L selectin, LFA-1, VLA-4, and ICAM-1) were measured by flow cytometry in a cross-sectional study of 100 HIV-infected and 49 HIV-seronegative adults. HIV-infected adults had lower numbers of CD3+ lymphocytes expressing L selectin (P < 0.0001) and VLA-4 (P < 0.01) and higher numbers of CD3+ lymphocytes expressing LFA-1bright (P < 0.002) than did HIV-negative adults. By CD4+-lymphocyte count category (>500, 200 to 500, or <200 cells/μl), HIV-infected adults with more advanced disease had lower percentages of CD3+ lymphocytes expressing L selectin and VLA-4 and higher percentages of CD3+ lymphocytes expressing LFA-1. The percentages of CD3+ CD28+ lymphocytes and of CD3+L selectin+ lymphocytes were positively correlated (Spearman coefficient = 0.86; P < 0.0001), and the percentage of CD3+ CD28+ lymphocytes and the CD3+ LFA-1bright lymphocyte/CD3+LFA-1dim lymphocyte ratio were negatively correlated (Spearman coefficient = −0.92; P <0.00001). The results of this study suggest that HIV infection is associated with altered expression of adhesion molecules.
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Prianggandanni, Made Ayu Vita, Anak Agung Wiradewi Lestari, I. Nyoman Wande, Ni Nyoman Mahartini, and Sianny Herawati. "Correlation between T-lymphocyte CD4+ and Total Lymphocyte Count (TLC), hemoglobin, Neutrophil to Lymphocyte Ratio (NLR) and T-lymphocyte CD4+/CD8+ ratio in HIV patients at Prof. Dr. I.G.N.G Ngoerah Hospital, Denpasar, Bali, Indonesia." Bali Medical Journal 12, no. 2 (June 24, 2023): 2017–21. http://dx.doi.org/10.15562/bmj.v12i2.4342.
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Background: Human Immunodeficiency Virus (HIV) is an RNA virus from the Retroviridae family, Lentiviri subfamily, which attacks the immune system, especially T lymphocytes, namely Cluster of Differentiation 4+ (CD4+) cells. Human Immunodeficiency Virus destroys T lymphocyte CD4+ cells, decreasing immunity against opportunistic infections. For monitoring of HIV, an examination of T lymphocyte CD4+ cells and complete blood counts were conducted. Methods: A cross-sectional quantitative analytic study was conducted from October 2021 to January 2022 at Prof. Dr. IGNG Ngoerah Hospital. Measurements were made on the total number of lymphocytes, hemoglobin levels, neutrophil-to-lymphocyte ratio (NLR), CD4+ levels and CD4+/CD8+ ratios. We analyze normality data using Kolmogorov-Smirnov and correlation using Pearson and Spearman tests. The p-value < 0.05 was considered significant. Results: 56 patients met the inclusion and exclusion criteria, with 46 males (82.1%) and 10 females (17.9%). Mean age 38.98±11.58 years, mean total lymphocyte 0.64 x 103 μL, median T lymphocyte CD4+ 133.50 sel/mm3, mean hemoglobin 10.11±1.49 g/dL, median NLR 6.51, median CD4+/CD8+ ratio 0.06. The hemoglobin variable was normally distributed, while the other variables were abnormal. The Pearson Correlation test showed a significant relationship between T lymphocytes CD4+ and hemoglobin with r=0.329 (p=0.013). Spearman's Correlation test showed a significant relationship between T lymphocytes CD4+ and NLR, total lymphocytes, CD4+/CD8+ ratio with r-0.334 (p=0.012), r=0.777 (p=0.000), r=0.729 (p=0.000) respectively. Conclusion: There is a strong and significant correlation between the level of T lymphocytes CD4+ and total lymphocyte count and the ratio of CD4+/CD8+, a weak and significant correlation between the level of T lymphocytes CD4+ with hemoglobin and NLR in HIV patients at Prof. Dr. IGNG Ngoerah Hospital.
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Janker, Stefanie, Simon Doswald, Roman R. Schimmer, Urs Schanz, Wendelin J. Stark, Martin Schläpfer, and Beatrice Beck-Schimmer. "Targeted Large-Volume Lymphocyte Removal Using Magnetic Nanoparticles in Blood Samples of Patients with Chronic Lymphocytic Leukemia: A Proof-of-Concept Study." International Journal of Molecular Sciences 24, no. 8 (April 19, 2023): 7523. http://dx.doi.org/10.3390/ijms24087523.
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In the past, our research group was able to successfully remove circulating tumor cells with magnetic nanoparticles. While these cancer cells are typically present in low numbers, we hypothesized that magnetic nanoparticles, besides catching single cells, are also capable of eliminating a large number of tumor cells from the blood ex vivo. This approach was tested in a small pilot study in blood samples of patients suffering from chronic lymphocytic leukemia (CLL), a mature B-cell neoplasm. Cluster of differentiation (CD) 52 is a ubiquitously expressed surface antigen on mature lymphocytes. Alemtuzumab (MabCampath®) is a humanized, IgG1κ, monoclonal antibody directed against CD52, which was formerly clinically approved for treating chronic lymphocytic leukemia (CLL) and therefore regarded as an ideal candidate for further tests to develop new treatment options. Alemtuzumab was bound onto carbon-coated cobalt nanoparticles. The particles were added to blood samples of CLL patients and finally removed, ideally with bound B lymphocytes, using a magnetic column. Flow cytometry quantified lymphocyte counts before, after the first, and after the second flow across the column. A mixed effects analysis was performed to evaluate removal efficiency. p < 0.05 was defined as significant. In the first patient cohort (n = 10), using a fixed nanoparticle concentration, CD19-positive B lymphocytes were reduced by 38% and by 53% after the first and the second purification steps (p = 0.002 and p = 0.005), respectively. In a second patient cohort (n = 11), the nanoparticle concentration was increased, and CD19-positive B lymphocytes were reduced by 44% (p < 0.001) with no further removal after the second purification step. In patients with a high lymphocyte count (>20 G/L), an improved efficiency of approximately 20% was observed using higher nanoparticle concentrations. A 40 to 50% reduction of B lymphocyte count using alemtuzumab-coupled carbon-coated cobalt nanoparticles is feasible, also in patients with a high lymphocyte count. A second purification step did not further increase removal. This proof-of-concept study demonstrates that such particles allow for the targeted extraction of larger amounts of cellular blood components and might offer new treatment options in the far future.
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Jiang, Weiming, Laiyi Kang, Hong-Zhou Lu, Xiaozhang Pan, Qingneng Lin, Qichao Pan, Yile Xue, Xinhua Weng, and Yi-Wei Tang. "Normal Values for CD4 and CD8 Lymphocyte Subsets in Healthy Chinese Adults from Shanghai." Clinical Diagnostic Laboratory Immunology 11, no. 4 (July 2004): 811–13. http://dx.doi.org/10.1128/cdli.11.4.811-813.2004.
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ABSTRACT The aim of this study was to establish reference ranges for lymphocyte subsets in Chinese adults. Venous blood specimens were obtained from 614 healthy, human immunodeficiency virus (HIV)-seronegative adults in Shanghai. Flow cytometry was used to determine percentages and absolute numbers of CD4 and CD8 T lymphocytes. Mean values for CD4 and CD8 lymphocytes were 727 and 540 cells/μl, respectively, yielding a CD4/CD8 ratio of 1.49. While CD8 lymphocyte values varied with age and gender, no significant differences in CD4 lymphocyte values were observed. Shanghai adults had approximately 100 fewer CD4 lymphocytes/μl on average than Caucasians, suggesting that lower CD4 lymphocyte cutoffs for classifying and monitoring HIV infection may be needed in China.
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Lucivero, G., G. Pierucci, and L. Bonomo. "Lymphocyte subsets in peripheral blood and pleural fluid." European Respiratory Journal 1, no. 4 (April 1, 1988): 337–40. http://dx.doi.org/10.1183/09031936.93.01040337.
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We have examined the distribution of B and T lymphocytes, T-cells with helper/inducer (T4+) or suppressor/cytotoxic (T8+) phenotypes and a subset of cells with natural killer (NK) activity and positive for the Leu 7 (HNK-1) surface antigen in peripheral blood and in lymphocyte-rich pleural effusions of patients with tuberculosis or malignancies (mesothelioma and lung cancer with pleural metastasis). In individual patients, the percentages of T lymphocytes were uniformly higher in pleural effusions than in peripheral blood; however, lower percentages of B lymphocytes and cells positive for the Leu 7 antigen were present in pleural fluids. The analysis of T-cell subpopulations demonstrated a selective enrichment of T lymphocytes with helper/inducer phenotype in pleural effusions, while the percentages of T-cells with suppressor/cytotoxic phenotype were similar in pleural fluid and peripheral blood. These results indicate that in lymphocytic pleural effusions the main lymphoid cell population is represented by T lymphocytes with helper/inducer phenotype, regardless of whether the effusion is due to tuberculosis or malignancies such as mesothelioma or lung cancer.
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Twigg, Homer L., Blake A. Spain, Diaa M. Soliman, Kenneth Knox, Richard A. Sidner, Carol Schnizlein-Bick, David S. Wilkes, and Gary K. Iwamoto. "Production of interferon-γ by lung lymphocytes in HIV-infected individuals." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 2 (February 1, 1999): L256—L262. http://dx.doi.org/10.1152/ajplung.1999.276.2.l256.
Full textAbstract:
A CD8+lymphocytic alveolitis occurs in up to 60% of asymptomatic human immunodeficiency virus (HIV)-infected individuals. Early in HIV infection, lymphocytes consist predominantly of cytotoxic T lymphocytes directed against HIV-infected targets. As HIV disease progresses, they are replaced by CD8+CD57+suppressor cells. Virus-specific cytotoxic T lymphocytes secrete interferon-γ (IFN-γ), an important cytokine in upregulating immune responses, primarily through macrophage activation. We examined the ability of lung and blood lymphocytes from HIV-positive patients at various stages of HIV infection to secrete IFN-γ spontaneously and in response to phytohemagglutinin A. IFN-γ production and secretion were determined with ELISA, Western blot, immunoprecipitation, and Northern blot techniques. Lung lymphocytes from HIV-infected individuals secreted large amounts of IFN-γ. However, this ability was lost in patients with late-stage disease. Correlation between blood and lung lymphocyte IFN-γ secretion was poor, suggesting regional differences in lymphocyte function. These data suggest that lung levels of IFN-γ are high until late in HIV disease. These findings support the concept of administering exogenous IFN-γ to patients with late-stage HIV disease and opportunistic infections.
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Kaur, Amitinder, Michele Di Mascio, Amy Barabasz, Michael Rosenzweig, Harold M. McClure, Alan S. Perelson, Ruy M. Ribeiro, and R. Paul Johnson. "Dynamics of T- and B-Lymphocyte Turnover in a Natural Host of Simian Immunodeficiency Virus." Journal of Virology 82, no. 3 (November 21, 2007): 1084–93. http://dx.doi.org/10.1128/jvi.02197-07.
Full textAbstract:
ABSTRACT Increased lymphocyte turnover is a hallmark of pathogenic lentiviral infection. To investigate perturbations in lymphocyte dynamics in natural hosts with nonpathogenic simian immunodeficiency virus (SIV) infection, the nucleoside analog bromodeoxyuridine (BrdU) was administered to six naturally SIV-infected and five SIV-negative sooty mangabeys. As a measure of lymphocyte turnover, we estimated the mean death rate by fitting a mathematical model to the fraction of BrdU-labeled cells during a 2-week labeling and a median 10-week delabeling period. Despite significantly lower total T- and B-lymphocyte counts in SIV-infected sooty mangabeys than in SIV-negative mangabeys, the turnover rate of B lymphocytes and CD4+ and CD8+ T lymphocytes was not increased in the SIV-infected animals. A small, rapidly proliferating CD45RA+ memory subset and a large, slower-proliferating CD45RA− central memory subset of CD4+ T lymphocytes identified in the peripheral blood of sooty mangabeys also did not show evidence of increased turnover in the context of SIV infection. Independently of SIV infection, the turnover of CD4+ T lymphocytes in sooty mangabeys was significantly higher (P < 0.01) than that of CD8+ T lymphocytes, a finding hitherto not reported in rhesus macaques or humans. The absence of aberrant T-lymphocyte turnover along with an inherently high rate of CD4+ T-lymphocyte turnover may help to preserve the pool of central memory CD4+ T lymphocytes in viremic SIV-infected sooty mangabeys and protect against progression to AIDS.
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Murakami, S., and H. Okada. "Lymphocyte-Fibroblast Interactions." Critical Reviews in Oral Biology & Medicine 8, no. 1 (January 1997): 40–50. http://dx.doi.org/10.1177/10454411970080010201.
Full textAbstract:
Chronic inflammatory reactions are usually characterized by inflammatory cell accumulation in the extravascular connective tissue. In such sites, inappropriate activation of circulating or resident lymphocytes becomes self-perpetuating and can lead to chronic tissue destruction. In addition to that, the locally infiltrated lymphocytes should have an opportunity to interact directly with fibroblasts composing the connective tissue. The direct interactions of those different cell types seem to play important roles in lymphocyte lodging and retention in such sites. Thus, for clarification of the immunopathogenesis of the chronic inflammatory diseases, including periodontitis, it is important that the molecular mechanisms involved in the heterotypic cell-cell interactions be revealed. In fact, it has been demonstrated that lymphocytes interact with various non-hematopoietic cells, such as epithelial cells and endothelial cells. Regarding interactions with fibroblasts, it has been shown that IFNγ-stimulated fibroblasts can regulate the proliferative responses of T-lymphocytes both positively and negatively. Furthermore, activated lymphocytes have demonstrated strong binding ability to various fibroblast cell lines. Blocking experiments utilizing monoclonal antibodies specific to various cell adhesion molecules revealed that very late antigen (VLA) integrins, lymphocyte-function-associated antigen (LFA-1)/intercellular adhesion molecule-1 (ICAM-1), CD44/hyarulonate are, at least in part, involved in lymphocyte-fibroblast interactions. In addition, recent findings raised the possibility that the adhesive interactions between lymphocytes and fibroblasts influenced the various cellular functions of each cell type. In fact, it was recently demonstrated that the adhesive interactions stimulated fibroblasts to increase expression of inflammatory cytokine mRNA. These results strongly suggest that fibroblasts are not merely innocent bystanders but actively participate in local inflammatory reactions by directly interacting with locally infiltrated lymphocytes.
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Dorward, D. "Interactions Between Mouse Lymphocytes And Borrelia Burgdorferi, The Infectious Agent Of Lyme Disease." Microscopy and Microanalysis 5, S2 (August 1999): 1242–43. http://dx.doi.org/10.1017/s143192760001953x.
Full textAbstract:
Lyme disease is a tick borne, multi-system disorder caused by low density systemic infections with the spirochete Borrelia burgdorferi. Without antimicrobial treatment, mammalian infections with these bacteria are persistent and chronic. Recent studies showed that B. burgdorferi can target, invade, and lyse both cultured and primary human B and T cells. Direct interactions between the spirochetes and lymphocytes also leads to adherence of B and T cell antigens on the surface of significant proportions of the bacteria . Adherent lymphocytic antigens inhibit binding of antibodies to prominent B. burgdorferi proteins, and interfere with classic complement-mediated killing, suggesting a possible role for spirochete-lymphocyte interactions in immune evasion.In order to develop an experimental animal model for assessing spirochete-lymphocyte interactions, B. burgdorferi and primary mouse lymphocytes were co-incubated and examined by electron microscopy. Mononuclear cells were separated from fresh mouse blood by Ficoll gradient centrifugation (ICN, Biomedicals, Aurora, Ohio).
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Gundersen, D., C. Trân-Thang, B. Sordat, F. Mourali, and C. Rüegg. "Plasmin-induced proteolysis of tenascin-C: modulation by T lymphocyte-derived urokinase-type plasminogen activator and effect on T lymphocyte adhesion, activation, and cell clustering." Journal of Immunology 158, no. 3 (February 1, 1997): 1051–60. http://dx.doi.org/10.4049/jimmunol.158.3.1051.
Full textAbstract:
Abstract Proteolysis and remodeling of the extracellular matrix occur physiologically in processes such as tissue morphogenesis and repair and may participate in the regulation of complex cell functions, including proliferation and differentiation. While matrix degradation appears to be relevant to T lymphocyte migration through tissues, little is known about whether degraded matrix affects T lymphocyte function. We have studied the interaction between T lymphocytes and tenascin-C (TN-C), a matrix protein we have previously reported to inhibit T lymphocyte activation, in the context of plasmin-induced degradation. Here we report that plasmin efficiently cleaves TN-C. Peripheral blood T lymphocytes stimulated with phorbol ester, anti-CD28, or anti-CD3 Ab, induce, within 24 to 48 h, a strong plasminogen-dependent proteolysis of TN-C. We demonstrate that stimulated T lymphocytes activate plasminogen by secreting the urokinase-type plasminogen activator (u-PA). Plasminogen activation by T lymphocyte-derived u-PA occurs efficiently in fluid phase in the absence of cells. We investigate the consequences of plasmin-induced proteolysis on three of the effects of TN-C in relation to lymphocyte functions. Plasmin proteolysis converts TN-C from a nonadhesive into an adhesive substrate for T lymphocytes and abolishes its aggregating activity on PBMC. In contrast, the inhibitory effect of TN-C on T lymphocyte activation remains unaffected. These observations demonstrate that stimulated T lymphocytes induce plasminogen-dependent proteolysis of TN-C by secreting u-PA and suggest that proteolysis of TN-C may represent a mechanism by which to regulate some of its effects on T lymphocyte functions.
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Lin, Jing, Huacai Zhao, Fuyong Jiao, Lei Ma, Weiqing Wang, and Le Ma. "Lymphocyte Hydrogen Sulfide Production Predicts Coronary Artery Lesions in Children with Kawasaki Disease: A Preliminary, Single-Center Study." Journal of Tropical Pediatrics 66, no. 2 (July 13, 2019): 171–77. http://dx.doi.org/10.1093/tropej/fmz047.
Full textAbstract:
Abstract To identify whether lymphocyte hydrogen sulfide production is a potential biomarker for predicting coronary artery lesions (CAL) in children with Kawasaki disease (KD). Eighty-six children with KD, 33 normal children and 43 children with fever from June 2016 to January 2019 in Shaanxi Provincial People's Hospital were enrolled. Of 86 KD patients, 16 patients exhibited CAL. Lymphocyte hydrogen sulfide production was significantly greater in KD patients (13.7 ± 2.7) nmol/min/108 lymphocytes than in the controls (9.26 ± 3.33) nmol/min/108 lymphocytes and the fever group (8.21 ± 2.77) nmol/min/108 lymphocytes. The lymphocyte hydrogen sulfide production was greater in CAL patients than the non-CAL patients [(16.24 ± 1.81) vs. (13.12 ± 2.58), p < 0.001]. Receiver operating characteristic curve indicated when the lymphocyte hydrogen sulfide production was >15.285 nmol/min/108 lymphocytes, the sensitivity and specificity for predicting CAL at convalescence were 87.5% and 82.9%, respectively. Lymphocyte hydrogen sulfide production in the acute period is a potentially useful biomarker for predicting CAL in KD children.
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Issekutz, T. B. "Effects of six different cytokines on lymphocyte adherence to microvascular endothelium and in vivo lymphocyte migration in the rat." Journal of Immunology 144, no. 6 (March 15, 1990): 2140–46. http://dx.doi.org/10.4049/jimmunol.144.6.2140.
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Abstract The first step in the migration of lymphocytes out of the blood is adherence of lymphocytes to endothelial cells (EC) in the postcapillary venule. It is thought that in inflammatory reactions cytokines activate the endothelium to promote lymphocyte adherence and migration into the inflammatory site. Injection of IFN-gamma, IFN-alpha/beta, and TNF-alpha into the skin of rats stimulated the migration of small peritoneal exudate lymphocytes (sPEL) into the injection site, and these cytokines mediated lymphocyte recruitment to delayed-type hypersensitivity, sites of virus injection, and in part to LPS. The effect of cytokines on lymphocyte adherence to rat microvascular EC was examined. IFN-gamma, IFN-alpha/beta, IL-1, TNF-alpha, and TNF-beta increased the binding of small peritoneal exudate lymphocyte (sPEL) to EC. IFN-gamma was more effective and stimulated adherence at much lower concentrations than the other cytokines. IL-2 did not increase lymphocyte adherence. LPS strongly stimulated lymphocyte binding. Treatment of EC, but not sPEL, enhanced adhesion, and 24 h of treatment with IFN-gamma and IL-1 induced near maximal adhesion. Lymph node lymphocytes, which migrate poorly to inflammatory sites, adhered poorly to unstimulated and stimulated EC, whereas sPEL demonstrated significant spontaneous adhesion which was markedly increased by IFN-gamma, IL-1, and LPS. Spleen lymphocytes showed an intermediate pattern of adherence. Combinations of IFN-gamma and TNF-alpha were additive in stimulating sPEL-EC adhesion. Depletion of sPEL and spleen T cells by adherence to IFN-gamma stimulated EC decreased the in vivo migration of the lymphocytes to skin sites injected with IFN-gamma, IFN-alpha/beta, TNF-alpha, poly I:C, LPS, and to delayed-type hypersensitivity reactions by 50%, and significantly increased the migration of these cells to normal lymph nodes, as compared to unfractionated lymphocytes. Thus the cytokines and lymphocytes involved in migration to cutaneous inflammation in the rat stimulate lymphocyte adhesion to rat EC in vitro, and IFN-gamma stimulated EC appear to promote the selective adhesion of inflammatory site-seeking lymphocytes.
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Clark, P., DE Normansell, DJ Innes, and CE Hess. "Lymphocyte subsets in normal bone marrow." Blood 67, no. 6 (June 1, 1986): 1600–1606. http://dx.doi.org/10.1182/blood.v67.6.1600.1600.
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Abstract Bone marrow aspirates and biopsies from ten normal donors were stained directly with monoclonal antibodies specific for lymphocyte, monocyte, and myeloid antigens, and were analyzed by flow cytometry. To avoid cell loss, lymphocytes were not specifically isolated prior to staining. T cells comprised 46% of aspirate lymphocytes and 22% of biopsy lymphocytes. Further, the Leu-3:Leu-2 ratio of bone marrow T cells was below 1.0. B cells comprised 8% to 11% of bone marrow lymphocytes in both aspirates and biopsies, and there was a substantial percentage of cells in the lymphocyte window that was negative for all B and T cell markers. The lymphocyte window had very little myeloid contamination; however, when the myeloid window was examined, staining was greater than 90%.