Academic literature on the topic 'CD62L'
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Journal articles on the topic "CD62L"
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Puc, Irwin, Tzu-Chuan Ho, Ko-Lun Yen, Amrita Vats, Jih-Jin Tsai, Po-Lin Chen, Yu-Wen Chien, Yu-Chih Lo, and Guey Chuen Perng. "Cytokine Signature of Dengue Patients at Different Severity of the Disease." International Journal of Molecular Sciences 22, no. 6 (March 12, 2021): 2879. http://dx.doi.org/10.3390/ijms22062879.
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Clinical presentations of dengue fever (DF) are diverse and non-specific, causing unpredictable progression and outcomes. Its progression and severity have been associated with cytokine levels alteration. In this study, dengue patients were classified into groups following the 2009 WHO dengue classification scheme to investigate the cytokine signature at different severity of the disease: dengue without warning sign symptoms (A); dengue with warning signs (B); severe dengue (C); other fever (OF) and healthy (Healthy). We analyzed 23 different cytokines simultaneously, namely IL-1b, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, IL-17A, IL-33, CD14, CD54, CD62E, CD62L, CD62p, CD106, CD121b, CD154, CD178, GM-CSF, IFN-g, MIF, ST2 and TNF from patients admitted to National Cheng Kung University Hospital during the 2015 Taiwan dengue outbreak. Cytokines TNF, CD54, CD62E, CD62L, CD62P, GM-CSF, IL-1b, IL-2, IL-6, IL-8, IL-10, IL-12p70, IL-17A, INF-g and MIF were elevated while CD106, CD154, IL-4 and L-33 were decreased when compared to the control. IL-10 demonstrated to be a potential diagnostic marker for DF (H and A group; AUC = 0.944, H and OF group; AUC = 0.969). CD121b demonstrated to be predictive of the SD (A and B group; AUC = 0.744, B and C group; AUC = 0.775). Our results demonstrate the cytokine profile changes during the progression of dengue and highlight possible biomarkers for optimizing effective intervention strategies.
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Pelikan, Zdenek. "Expression of Surface Markers on the Blood Cells during the Delayed Asthmatic Response to Allergen Challenge." Allergy & Rhinology 5, no. 2 (January 2014): ar.2014.5.0087. http://dx.doi.org/10.2500/ar.2014.5.0087.
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Patients with bronchial asthma develop various types of asthmatic response to bronchial challenge with allergen, such as immediate/early asthmatic response (IAR), late asthmatic response (LAR) or delayed asthmatic response (DYAR), because of different immunologic mechanisms. The DYAR, occurring between 24 and 56 hours after the bronchial allergen challenge (p < 0.01), differs from IAR and LAR in clinical as well as immunologic features. This study investigates the expression of CD molecules (markers) on the surface of particular cell populations in the peripheral blood and their changes during the DYAR. In 17 patients developing the DYAR (p < 0.01), the bronchial challenge with allergen was repeated 2–6 weeks later. The repeated DYAR (p < 0.001) was combined with recording of CD molecule expression on various types of blood cells by means of flow cytometry up to 72 hours after the challenge. The results were expressed in percent of the mean relative fluorescence intensity. The DYAR was accompanied by (a) increased expression of CD11b, CD11b/18, CD16, CD32, CD35, CD62E, CD62L, CD64, and CD66b on neutrophils; CD203C on basophils; CD25and CD62L on eosinophils; CD14, CD16, CD64, and CD86 on monocytes; CD3, CD4, CD8, CD11a, CD18, and CD69 on lymphocytes; CD16, CD56, CD57, and CD94 on natural killer (NK) cells; and CD31, CD41, CD61, CD62P, and CD63 on thrombocytes and (b) decreased expression of CD18 and CD62L on eosinophils, CD15 on neutrophils, and CD40 on lymphocytes. These results suggest involvement of cell-mediated hypersensitivity mechanism, on participation of Th1- lymphocytes, neutrophils, monocytes, NK cells, and thrombocytes in the DYAR.
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Cerqueira, Bruno Antônio Veloso, Wendell Vilas Boas, Magda Oliveira Seixas, Elder Trindade Damasceno, Cyntia Cajado Souza, Mitermayer Galvão Reis, and Marilda Souza Goncalves. "Expression Levels of CD11b, CD18, CD32, CD62L (L-Selectin) and CD62P (P-Selectin) and Its Role in Sickle Cell Anemia Inflammatory State." Blood 112, no. 11 (November 16, 2008): 2504. http://dx.doi.org/10.1182/blood.v112.11.2504.2504.
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Abstract Vascular occlusions (VOC) underlie most of the acute and chronic sickle cell anemia (SCA) clinical complications and have been correlated to soluble adhesion molecules up regulation and leukocyte activation. A sequential process involving adhesion through selectins and integrins governs leukocyte recruitment to activated endothelium and to sickle red blood cells (RBC), resulting in heterotypic aggregation and VOC. The chronic hemolysis is the major cause of oxidative stress and it can induce transcriptions factors involved in the recruitment of adherent leukocytes in venules. In this work, we assessed the inflammatory potential of leukocytes in venous blood samples by examining cell surface antigens expression by flow cytometry, activation state and its association with hemolytic state in SCA patients group. The study was approved by the FIOCRUZ ethical committee and informed consents were signed by patients or official responsible. Leukocytes were obtained from 22 SCA patients and 22 healthy controls after RBC lyses and labeled with monoclonal anti-CD11b, anti-CD18, anti-CD32, anti-CD62L (L-Selectin) and anti-CD62P (P-Selectin). Leukocyte activation was stimulated by LPS. Statistical analyses were performed using SPSS version 9.0. The basal expression levels on leukocytes cell surface antigens from patients were not different from the control group. However, the CD62L expression levels were associated to C-reactive protein (CRP) higher levels and decrease of fetal hemoglobin in SCA patients (p=0.012). The SCA patients had higher CRP levels when compared to reference levels. Moreover, the data showed a co-expression of CD11b with CD18 (p<0.0001) and CD62P (p=0.011).The platelet count was positively correlated to CD11b expression (p=0.016) and the alanine transaminase high levels with the CD62P expression (p=0.012). Our results demonstrate a leukocyte chronic activation state by expression of CD62L related to CRP higher levels. Interestingly, the platelets could be activated by the indirect activation of CD62P by CD11b, participating of the inflammation state presents at vaso-occlusive events. It seems that the stress oxidative generated by the hemolytic state can contribute to endothelial dysfunction and vaso-occlusive events by CD62L activation in SCA. Fetal hemoglobin is a prognostic factor for several sickle cell complications and we showed that it can ameliorate the CD62L expression on leukocytes, decreasing the chronic inflammatory state of this disease. CD62L serves to as a homing receptor for naïve T lymphocytes and dendritic cells to lymph nodes, mediating the biding of T cells to high endothelial venules, in this view, this can be important marker to inflammatory state and vascular complications in SCA.
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Howard, C. J. "Ruminant cluster CD62L." Veterinary Immunology and Immunopathology 52, no. 4 (August 1996): 255–56. http://dx.doi.org/10.1016/0165-2427(96)05571-7.
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Burgess, Melinda, Peter Mollee, Richa Singhania, Catherine Cheung, Lynne Chambers, Reynolds Brent, Louise Smith, Nicholas Saunders, Nigel McMillan, and Devinder S. Gill. "CD62L Expression Is Associated With Chronic Lymphocytic Leukemia (CLL) Cell Survival In Vitro and Represents a Novel Therapeutic Target In CLL." Blood 122, no. 21 (November 15, 2013): 4136. http://dx.doi.org/10.1182/blood.v122.21.4136.4136.
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Abstract Background Recent advances in the treatment of chronic lymphocytic leukemia (CLL) have improved overall patient survival, however, the disease remains incurable. There is accumulating evidence that CLL cell resistance to apoptosis is attributable to microenvironmental factors mediated by cell-cell interactions and dysregulation of cytokine signals. Despite this resistance to apoptosis in vivo, CLL cells undergo rapid spontaneous apoptosis when removed from the body. Recently, we and others have demonstrated that this in vitro apoptosis could be reduced by culture of CLL cells at high density and/or in the presence of accessory and stromal cells. A growing body of evidence indicates that alterations in the adhesion properties of neoplastic cells play a pivotal role in the development and progression of CLL. Methods and Results To dissect the complex microenvironmental interactions present in vitro,we profiled the immunophoenotypic changes that occur in long-term CLL PBMC cultures using flow cytometry. Significant changes were observed for 25 antigens, with increases observed in the expression of CD26, CD40, CD58, CD62L and CD103 and decreased expression observed in CD11c, CD32, CD49f, CD62P, CD80, CD106, CD140a, CD141, CD184, CD206 and CD273. The most highly upregulated marker was CD62L (L-selectin, a homing receptor thought to play a role in CLL cell trafficking) and this expression was confirmed in a further subset of patient samples. Using confocal microscopy CD62L expression was present in proliferation and survival niches involved in CLL in the bone marrow and lymph nodes. The pro-survival role of CD62L was examined using a functional blocking antibody which resulted in the significant loss of CLL cell survival. PBMCs from normal healthy controls were unaffected by CD62L antibody treatment, which reinforces that the response is restricted to CLL cells. Furthermore, CD62L antibody treatment caused a specific reduction of CD5+/CD19+ cells with a 49% reduction when compared to untreated PBMCs. This cytotoxic mediated response of CD62L blockade was not abrogated by the presence of stromal cell line HS-5, or endothelial cell line HUVECs suggesting that anti-CD62L therapy may be effective in vivo where pro-survival microenvironmental interactions are intact. We also demonstated a significant increase in cytotoxic responses when anti-CD62L treatment was combined with both fludarabine and mafosfamide compared to either each agent alone, or any two agents combined. Conclusion Immunophenotypic analysis of CLL cultures demonstrated that the expression of several cell surface markers change throughout in vitro culture. These markers are suggestive of cell-cell interactions that clearly provide survival signals. Blocking the activation and homing marker, CD62L, regulates CLL cell survival in vitro and induces cell death equivalent to current CLL chemotherapeutics. Overall, CD62L is a novel prosurvival effector that may represent an attractive therapeutic target in CLL. Disclosures: No relevant conflicts of interest to declare.
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Xu, Heping, Ayyakkannu Manivannan, Isabel Crane, Rosemary Dawson, and Janet Liversidge. "Critical but divergent roles for CD62L and CD44 in directing blood monocyte trafficking in vivo during inflammation." Blood 112, no. 4 (August 15, 2008): 1166–74. http://dx.doi.org/10.1182/blood-2007-06-098327.
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Abstract Using noninvasive in vivo imaging and experimental autoimmune uveoretinitis as a model, we show for the first time that the mechanisms controlling blood monocyte recirculation through peripheral and lymphoid tissues alter during inflammation. The recirculation of monocytes in mice with ocular inflammation but not controls was found to depend on the selectin CD62-ligand (CD62L) and on CD44. Not only was rolling efficiency ablated or markedly reduced in antibody-treated mice, but most of the labeled monocytes also disappeared from the circulation within seconds, anti-CD44–treated monocytes homing to the lymph nodes and anti–CD62L-treated monocytes homing to the spleen. Our data indicate that, although PSGL-1 has a partial role in the transmigration of monocytes into the inflamed retina, CD62L has a key role in regulating recruitment of monocytes to lymphoid tissue from the blood during inflammation and that CD44 is required to maintain CD62L+ inflammatory monocytes within the circulation during inflammation. This effect was systemic, because sequestered monocytes accumulated in mesenteric as well as draining cervical lymph nodes, and inflammation dependent, because depletion of circulating blood monocytes was much reduced or absent in normal mice and accumulations of adoptively transferred monocytes in the lymphoid tissues did not occur.
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Nesterova, I. V., V. V. Malinovskaya, S. V. Khaydukov, D. L. Nguyen Thi, G. A. Chudilova, and L. V. Lomtatidze. "DIFFERENTIATED EFFECTS OF GLUCOSAMINYLMURAMILDIPEPTIDE ON THE NONTRANSFORMED AND EXPERIMENTALLY TRANSFORMED PHENOTYPE OF CD62L+CD63+CD66d+ NEUTROPHILIC GRANULOCYTES IN CONVENTIONALLY HEALTHY PEOPLE." Medical Immunology (Russia) 20, no. 6 (December 15, 2018): 847–54. http://dx.doi.org/10.15789/1563-0625-2018-6-847-854.
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Modern studies have shown a high plasticity and phenotypic diversity of neutrophilic granulocytes (NG) provided by different receptors, which are diagnostic markers for the functional capacity of the cell in the course of their activities. We investigated NG from peripheral blood, obtained from healthy people of both sexes aged from 26 to 66 years. Evaluation of the neutrophil membrane receptor expression was carried out by flow cytometry. The relative amount of neutrophilic granulocytes expressing membrane CD62L, CD63, CD66d receptors and the intensity of their expression were determined according to their fluorescence intensities. The surface NG membrane receptors, i.e., CD62L, CD63, CD66d were studied upon the in vitro experimental influence of the following bacterial peptides: N-formyl-methionyl-leucyl-phenylalanine (FMLP, model 1); glucosaminylmuramyldipeptide (GMDP, model 2), and simultaneous incubation of NG blood with fMLP and GMDP (model 3). The in vitro treatment with fMLP in the in vitro model was used to transform the NG phenotype of conventionally healthy subjects, expressing CD62, CD63, CD66d molecules. The treatment caused a significantly decrease in both CD62L and the CD62L expression in relative amounts of neutrophilic granulocytes with a parallel increase of CD63 expression density. The effect of GMDP on the NG phenotype of conditionally healthy subjects did not change the amount of CD62L+NG and CD63+NG, and did not affect CD62L and CD63 expression density on the surface of NG. However, the amount of CD66d+NG was significantly increased with the unchanged expression of CD66d molecules. GMDP introduced together with the bacterial fMLP peptide was shown to neutralize some features of the NG phenotype transformation caused by fMLP, i.e., the amount of CD62L+ NG was restored by 22 % and the CD62L expression density increased significantly. At the same time, GMDP did not correct the negative effect of fMLP upon the number of CD63+NG and CD66d+NG, and on the CD63 and CD66d expression. Simultaneous addition of fMLP and GMDP did significantly increase the amount of CD66d+NG and expression density of CD63 molecules on the CD63+NG membrane as compared to intact NG of conditionally healthy subjects. The obtained data are important in order to justify some new immunotherapeutic strategies aimed at correction of the negatively transformed NG phenotype, which accompanies some infectious and inflammatory diseases of bacterial etiology with atypical clinical course.
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Drescher, Hannah K., Angela Schippers, Stefanie Rosenhain, Felix Gremse, Laura Bongiovanni, Alain de Bruin, Sreepradha Eswaran, et al. "L-Selectin/CD62L Is a Key Driver of Non-Alcoholic Steatohepatitis in Mice and Men." Cells 9, no. 5 (April 29, 2020): 1106. http://dx.doi.org/10.3390/cells9051106.
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CD62L (L-Selectin) dependent lymphocyte infiltration is known to induce inflammatory bowel disease (IBD), while its function in the liver, especially in non-alcoholic steatohepatitis (NASH), remains unclear. We here investigated the functional role of CD62L in NASH in humans as well as in two mouse models of steatohepatitis. Hepatic expression of a soluble form of CD62L (sCD62L) was measured in patients with steatosis and NASH. Furthermore, CD62L−/− mice were fed with a methionine and choline deficient (MCD) diet for 4 weeks or with a high fat diet (HFD) for 24 weeks. Patients with NASH displayed increased serum levels of sCD62L. Hepatic CD62L expression was higher in patients with steatosis and increased dramatically in NASH patients. Interestingly, compared to wild type (WT) mice, MCD and HFD-treated CD62L−/− mice were protected from diet-induced steatohepatitis. This was reflected by less fat accumulation in hepatocytes and a dampened manifestation of the metabolic syndrome with an improved insulin resistance and decreased cholesterol and triglyceride levels. Consistent with ameliorated disease, CD62L−/− animals exhibited an enhanced hepatic infiltration of Treg cells and a strong activation of an anti-oxidative stress response. Those changes finally resulted in less fibrosis in CD62L−/− mice. Additionally, this effect could be reproduced in a therapeutic setting by administrating an anti-CD62L blocking antibody. CD62L expression in humans and mice correlates with disease activity of steatohepatitis. CD62L knockout and anti-CD62L-treated mice are protected from diet-induced steatohepatitis suggesting that CD62L is a promising target for therapeutic interventions in NASH.
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Vassena, Lia, Erica Giuliani, Herwig Koppensteiner, Sebastian Bolduan, Michael Schindler, and Margherita Doria. "HIV-1 Nef and Vpu Interfere with L-Selectin (CD62L) Cell Surface Expression To Inhibit Adhesion and Signaling in Infected CD4+T Lymphocytes." Journal of Virology 89, no. 10 (March 11, 2015): 5687–700. http://dx.doi.org/10.1128/jvi.00611-15.
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ABSTRACTLeukocyte recirculation between blood and lymphoid tissues is required for the generation and maintenance of immune responses against pathogens and is crucially controlled by the L-selectin (CD62L) leukocyte homing receptor. CD62L has adhesion and signaling functions and initiates the capture and rolling on the vascular endothelium of cells entering peripheral lymph nodes. This study reveals that CD62L is strongly downregulated on primary CD4+T lymphocytes upon infection with human immunodeficiency virus type 1 (HIV-1). Reduced cell surface CD62L expression was attributable to the Nef and Vpu viral proteins and not due to increased shedding via matrix metalloproteases. Both Nef and Vpu associated with and sequestered CD62L in perinuclear compartments, thereby impeding CD62L transport to the plasma membrane. In addition, Nef decreased total CD62L protein levels. Importantly, infection with wild-type, but not Nef- and Vpu-deficient, HIV-1 inhibited the capacity of primary CD4+T lymphocytes to adhere to immobilized fibronectin in response to CD62L ligation. Moreover, HIV-1 infection impaired the signaling pathways and costimulatory signals triggered in primary CD4+T cells by CD62L ligation. We propose that HIV-1 dysregulates CD62L expression to interfere with the trafficking and activation of infected T cells. Altogether, this novel HIV-1 function could contribute to virus dissemination and evasion of host immune responses.IMPORTANCEL-selectin (CD62L) is an adhesion molecule that mediates the first steps of leukocyte homing to peripheral lymph nodes, thus crucially controlling the initiation and maintenance of immune responses to pathogens. Here, we report that CD62L is downmodulated on the surfaces of HIV-1-infected T cells through the activities of two viral proteins, Nef and Vpu, that prevent newly synthesized CD62L molecules from reaching the plasma membrane. We provide evidence that CD62L downregulation on HIV-1-infected primary T cells results in impaired adhesion and signaling functions upon CD62L triggering. Removal of cell surface CD62L may predictably keep HIV-1-infected cells away from lymph nodes, the privileged sites of both viral replication and immune response activation, with important consequences, such as systemic viral spread and evasion of host immune surveillance. Altogether, we propose that Nef- and Vpu-mediated subversion of CD62L function could represent a novel determinant of HIV-1 pathogenesis.
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Che Mohd Nassir, Che Mohd Nasril, Mazira Mohamad Ghazali, Amanina Ahmad Safri, Usman Jaffer, Wan Zaidah Abdullah, Nur Suhaila Idris, and Mustapha Muzaimi. "Elevated Circulating Microparticle Subpopulations in Incidental Cerebral White Matter Hyperintensities: A Multimodal Study." Brain Sciences 11, no. 2 (January 20, 2021): 133. http://dx.doi.org/10.3390/brainsci11020133.
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Asymptomatic (or “silent”) manifestations of cerebral small vessel disease (CSVD) are widely recognized through incidental findings of white matter hyperintensities (WMHs) as a result of magnetic resonance imaging (MRI). This study aims to examine the potential associations of surrogate markers for the evaluation of white matter integrity in CSVD among asymptomatic individuals through a battery of profiling involving QRISK2 cardiocerebrovascular risk prediction, neuroimaging, neurocognitive evaluation, and microparticles (MPs) titers. Sixty asymptomatic subjects (mean age: 39.83 ± 11.50 years) with low to moderate QRISK2 scores were recruited and underwent neurocognitive evaluation for memory and cognitive performance, peripheral venous blood collection for enumeration of selected MPs subpopulations, and 3T MRI brain scan with specific diffusion MRI (dMRI) sequences inclusive of diffusion tensor imaging (DTI). WMHs were detected in 20 subjects (33%). Older subjects (mean age: 46.00 ± 12.00 years) had higher WMHs prevalence, associated with higher QRISK2 score and reduced processing speed. They also had significantly higher mean percentage of platelet (CD62P)- and leukocyte (CD62L)-derived MPs. No association was found between reduced white matter integrity—especially at the left superior longitudinal fasciculus (LSLF)—with age and neurocognitive function; however, LSLF was associated with higher QRISK2 score, total MPs, and CD62L- and endothelial cell-derived MPs (CD146). Therefore, this study establishes these multimodal associations as potential surrogate markers for “silent” CSVD manifestations in the well-characterized cardiocerebrovascular demographic of relatively young, neurologically asymptomatic adults. Furthermore, to the best of our knowledge, this study is the first to exhibit elevated MP counts in asymptomatic CSVD (i.e., CD62P and CD62L), which warrants further delineation.
Dissertations / Theses on the topic "CD62L"
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Gu, Baijun. "TWO PATHWAYS OF SHEDDING OF L-SELECTIN AND CD23 FROM HUMAN B-LYMPHOCYTES." University of Sydney, 2000. http://hdl.handle.net/2123/821.
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Lymphocytes from patients with B-chronic lymphocytic leukemia (B-CLL) express large numbers of P2X7 receptors for extracellular adenosine triphosphate (ATP). Activation of P2X7 receptors induces multiple downstream effects, of which the best documented is the opening of an ionic channel that is selective for divalent cations. Another effect of ATP is to induce the shedding of L-selectin (CD62L), a molecule which is involved in the adhesive interactions of lymphocytes on endothelial cells. High levels of soluble L-selectin and CD23 are found in the serum of patients with B-CLL, although the mechanisms involved in their production are poorly characterized. Because extracellular ATP causes shedding of L-selectin, we studied the effect of ATP on shedding of CD23, an adhesion molecule expressed on the surface of B-CLL lymphocytes. ATP induced the shedding of CD23 at an initial rate of 12% of that for L-selectin, while the EC50 of ATP (35 uM) and BzATP (10 uM) was identical for shedding of both molecules. Inactivation of the P2X7 receptor by pre-incubation with OxATP, an irreversible inhibitor of P2X7 purinoceptor, abolished ATP-induced shedding of both molecules. Moreover, KN-62, the most potent inhibitor for the P2X7 receptor inhibited ATP-induced shedding of both CD23 and L-selectin with the same IC50 (12 nM). Ro 31-9790, a membrane permeant zinc chelator which inhibits the phorbol-ester stimulated shedding of L-selectin also inhibited shedding of CD23 from B-CLL lymphocytes, but the IC50 was different for the two shed molecules (25 versus 1 ug/ml respectively). Although L-selectin was completely shed by incubation of cells with phorbol-ester no CD23 was lost under these conditions. Also, Ca2+ inhibits ATP-induced CD23 shedding but not L-selectin shedding. Since soluble CD23 and L-selectin are found in the serum of normal subjects and B-CLL patients, the expression of these two adhesion molecules on lymphocytes before and after transendothelial migration was studied in an in vitro model of this process. In normal and B-CLL subjects, 71�b5% of L-selectin from both T and B cells and 90% of CD23 from B cells was lost following transmigration, while the expression of a range of other adhesion molecules such as VLA-4, ICAM-1, LFA-1 and CD44 was unchanged. Lymphocytes incubated with OxATP retained their capacity for transendothelial migration and showed the same loss of L-selectin as control leukaemic lymphocytes. Ro 31-9790, which can protect ATP-induced both L-selectin and CD23 shedding, had no effect on inhibiting L-selectin and CD23 lost during transmigration. These data show the presence of a second pathway for the downregulation of L-selectin and CD23 from the lymphocyte surface. Data in vivo from 'knock-out' mice show that L-selectin is essential for the emigration of lymphocytes through high endothelial venules into lymph nodes. The migration of normal and B-CLL lymphocytes across confluent human umbilical vein endothelial monolayers was studied in an in vitro model of this process. Lymphocytes treated with ATP or BzATP showed 56�b25% or 67�b16% loss of L-selectin on the surface and 36�b24% or 64�b19% decrease of transmigration, respectively, while OxATP, which does not alter the L-selectin level, had no effect on lymphocyte transmigration. Further experiments examined this correlation between L-selectin expression and lymphocyte transendothelial migration in this model system. A quantitative assay for cell surface L-selectin showed that expression of L-selectin was lower on B-CLL lymphocytes (8,880�b5,700 molecules/cell) than on normal lymphocytes (29,500�b7,500 molecules/cell, p less than 0.001). Also the rate of transmigration of B-CLL lymphocytes (1.5�b0.9 migrated cells/HUVEC) was lower than normal peripheral lymphocytes (2.4�b0.9 migrated cells/HUVEC, p=0.04). Incubation of lymphocytes in complete medium for 24 hrs increased the expression of L-selectin on B-CLL lymphocytes by 1.5 to 2 fold while the normal lymphocyte L-selectin remained at the initial level. This upregulation of B-CLL L-selectin correlated with a 2 fold increased rate of transendothelial migration. A correlation was found between L-selectin expression on lymphocytes and their ability for transendothelial migration (r^2=0.6). This study shows that the adhesion molecules L-selectin and CD23 can be lost from lymphocytes by two different physiological pathways. One is by P2X7 receptor activation by extracellular ATP while the second is activated by transendothelial migration of these cells. A second finding is that B-CLL lymphocytes have lower level of L-selectin expression and an impaired ability for transendothelial migration compared with normal peripheral blood lymphocytes. Do these results explain the high serum levels of soluble L-selectin and CD23 observed in B-CLL? Although B-CLL lymphocytes do not recirculate as rapidly as normal peripheral blood lymphocytes, the greatly increased number of leukaemic cells in B-CLL ensures that much more soluble L-selectin and CD23 is generated during the recirculation of these cells through the body.
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Silva, Patrick Fernandes da. "Avaliação do efeito imunomodulador da lectina extraída de Brassica oleracea sobre neutrófilos." Universidade Federal de Viçosa, 2017. http://www.locus.ufv.br/handle/123456789/11605.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
Neutrófilos são as primeiras células do sistema imune a migrarem para o tecido inflamado e exercem a importante função de fagocitose e eliminação imediata de patógenos invasores. A ativação de neutrófilos é um processo de múltiplos passos e de alta complexidade. A busca por agentes biológicos capazes de modular o processo de ativação, migração, fagocitose e produção de espécies reativas de oxigênio (ROS) é importante pois aumentam a gama de opções para utilização na pesquisa. Nesse trabalho utilizamos a lectina extraída de Brassica oleracea (BOL) a fim de avaliar a sua capacidade na modulação da resposta de neutrófilos. Para os ensaios nós purificamos neutrófilos de camundongo tanto do sangue periférico quanto da cavidade peritoneal buscando avaliar sua capacidade migratória, o índice de CD62L na superfície e o índice fagocítico de neutrófilos pré-incubados com BOL. A lectina apresentou diversos efeitos de acordo com a dose utilizada, sendo possível observar o efeito de indução de migração para cavidade peritoneal de camundongos quando utilizada em doses intermediárias (1 μg/mL e 2,5 μg/mL) tanto quanto o efeito de redução de migração quando observada em doses altas (5 μg/mL e 10 μg/mL). O índice de fagocitose também foi avaliado e houve alteração de acordo também com a dose utilizada. As doses mais altas apresentaram efeito de redução na taxa de fagocitose (5 μg/mL e 10 μg/mL) enquanto as outras doses não apresentavam diferença estatística. Com esse trabalho conseguimos observar os efeitos imunomodulatórios sobre neutrófilos de uma lectina ainda muito pouco estudada e que demonstrou ter efeitos sobre a fisiologia de neutrófilos de acordo com a dose escolhida, alterando sua capacidade de migração e fagocitose.
Neutrophils are the first cells of the immune system to migrate into inflamed tissue and they develop the important function of phagocytosis and immediate elimination of invading pathogens. Neutrophil activation is a multi-step and highly complex process. Research on biological agents able to modulate the activation, migration, phagocytosis and production of reactive oxygen species (ROS) are important because they increase the range of options for use in the research. In this work we used the lectin extracted from Brassica oleracea (BOL) aiming to evaluate its ability to modulate the neutrophil response. For the tests, we purified mouse neutrophils from the peripheral blood and the peritoneal cavity with the objective to evaluate their migratory capacity, the surface CD62L index and the phagocytic index of neutrophils pre-incubated with BOL. The lectin presented several effects according to the dose used, being possible to observe the effect of induction of migration to peritoneal cavity when it was used in intermediate doses (1 μg/mL and 2.5 μg/mL) as well as the effect of reduction of migration as observed at high doses (5 μg/ mL and 10 μg/mL). The phagocytosis index was also evaluated and there was also an alteration according to the dose used. Higher doses showed a smaller phagocytosis rate (5 μg/mL and 10 μg/mL), unlike the other doses. In this work we were able to observe the immunomodulatory effects on neutrophils of a lectin that has not yet been studied and has shown to have effects on neutrophil physiology according to the chosen dose, altering its migration capacity and phagocytosis.
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Carrette, Florent. "Nouveaux modes de régulation du homing des lymphocytes T en aval de la PI3-Kinase et lors de l'infection par Mycobacterium ulcerans." Paris 6, 2010. http://www.theses.fr/2010PA066150.
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La voie de la PI3K contrôle la survie et participe à la prolifération des lymphocytes T (LT) en réponse à l'antigène. Les PI3K de classe IA sont composées d'une sous-unité régulatrice associée à une sous-unité catalytique et sont recrutées à la synapse immunologique en aval de l'angagement du TCR. Trois sous-unités régulatrices, p85α p55α et p50α, codées par le gène pik3r1 sont exprimées dans les LT. Nous avons montré que seule p85α est recrutée, via un mécanisme dépendant de son domaine N-terminal. En aval de la PI3K, Akt phosphoryle et inactive les facteurs de transcription FOXO. En plus de leur rôle dans le contrôle du cycle cellulaire, ils ont des rôles spécifiques de cellules. Nous avons montré que dans les LT, FOXO1 contrôle les gènes codant pour les protéines CD62L et S1P1, impliqués dans le homing des LT dans les ganglions lymphatiques. FOXO1 semble donc avoir une dualité fonctionnelle permettant à la fois l'adressage des LT dans les ganglions lymphatiques et leur expansion clonale restreinte à ces organes suite à la reconnaissance antigénique. Mycobacterium ulcerans, la bactérie responsable de l'ulcère de Buruli, échappe au système immunitaire grâce à la mycolactone qu'elle produit. Ce processus passe par l'inhibition du homing des LT dans les ganglions lymphatiques, ce qui réduit fortement la prolifération des LT en réponse un antigène spécifique. Ceci est dû à une neutralisation de l'expression de CD62L à la surface des LT, via le contrôle du miRNA Let-7b, et à une mobilité intra-ganglionnaire des LT réduite. Au-delà de l'intérêt de cette découverte dans la physiopathologie de l'ulcère de Buruli, la mycolactone pourrait constituer un nouvel immunosuppresseur.
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Maruya, Etsuko. "Evidence that CD31, CD49b, and CD62L are immunodominant minor histocompatibility antigens in HLA identical sibling bone marrow transplants." Kyoto University, 2001. http://hdl.handle.net/2433/150586.
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Mohammed, Rebar N. "The impact of L-selectin/CD62L on the co-stimulation and migration of CD8+ T cells during virus infection." Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/88514/.
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The strategy of the adaptive immune system in eliminating viruses from infected tissues is the activation of CD8+ T cells with specific T cell receptor in the LN draining the site of virus entry and subsequent migration of these cells to the sites of the viral infection. L-selectin, a well characterized LN homing receptor, is variably expressed on virus peptide activated CD8+ T cells, regulated through two separate mechanisms of early ectodomain shedding and late gene silencing. The role of L-selectin in homing of activated CD8+ T cells to sites of virus infection is not studies in detail. Here we show that despite being primed normally in the draining LN, there were a hierarchy in homing ability of adoptively transferred CD8+ T cells expressing mutant L-selectin(which resist shedding and gene silencing upon T cell activation), wildtype Lselectin and deficient in L-selectin (Ko) to the site of virus infection. The Lselectin specific recruitment was confirmed by using antibody blockade strategy and short-term competitive homing experiments. Furthermore, Lselectin dependent homing of virus specific CD8+ T cells rather than hyperfunctional or hyperproliferative T cells conferred anti-viral immunity against two evolutionarily distinct viruses, vaccinia and influenza viruses which infect mucosal and visceral organs, respectively.
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Jülke, Kerstin. "Role of cytokines for NK cell competence and differentiation." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16216.
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Humane NK Zellen können in CD56br und CD56dim NK Zellen unterteilt werden. In dieser Arbeit wurde untersucht, in welchem Zusammenhang die verschiedenen NK Zell Populationen stehen und wie funktional kompetente NK Zellen generiert werden. Des Weiteren wurde die Heterogenität der CD56dim NK Zell Population in Bezug auf Funktionalität und Differenzierungsstadien analysiert. Es konnte gezeigt werden, dass CD56br NK Zellen in CD56dim NK Zellen differenzieren. Währenddessen werden u.a. MHC-I spezifische inhibierende Rezeptoren (KIR) erworben. Diese sind essentiell für die Unterscheidung zwischen “Selbst” und “Nicht-Selbst”, wobei nur NK Zellen, die Selbst-MHC-spezifische KIRs tragen, funktional kompetent sind. In der vor-liegenden Arbeit konnte darüber hinaus gezeigt werden, dass zuvor anerge NK Zellen nach Zytokin-induzierter Expression eines Selbst-MHC-spezifischen KIRs kompetent werden. Ex vivo Analysen humaner Gewebe lassen vermuten, dass diese Prozesse während einer Entzündung in sekundären lymphatischen Organen (SLO) stattfinden könnten. Auch CD56dim NK Zellen selbst sind nicht homogen, hingegen können anhand der Expression von KIRs oder CD62L, welches für die Migration in SLO wichtig ist, weitere Subpopulationen unterschieden werden. Eine umfassende Analyse bezüglich KIR und CD62L Expression führte zur Identifizierung einer zuvor nicht charakterisierten CD56dimCD62L+ NK Zell Population, welche die Fähigkeiten von CD56br, Zytokine zu produzieren und zu proliferieren, mit einem hohen zytotoxischen Potenzial, vereinigt. Weitere ex vivo Untersuchungen des Phänotyps, der Telomerlängen und der Verteilung in Relation zum Alter lassen vermuten, dass die Differenzierung humaner NK Zellen von CD56br über CD56dimCD62L+ zu CD56dimCD62L- verläuft, wobei die Zellen mit fortschreitender Dif-ferenzierung ihre Fähigkeit auf Zytokine zu antworten verlieren und dafür die Fähigkeit er-langen, über aktivierende Rezeptoren stimuliert zu werden.Human NK cells comprise two main subsets, CD56br and CD56dim cells. In this study, an extensive analysis of human NK cell phenotype and functional characteristics has been performed in order to investigate the developmental relation between NK cell subsets, to elucidate how NK cell competence is acquired and to further dissect the heterogeneity of the CD56dim subset with regard to functions and differentiation history of human NK cells. It could be shown that upon cytokine activation, CD56br differentiate into CD56dim NK cells and that this process might take place in inflamed secondary lymphoid organs (SLO). One of the crucial markers acquired during this process is KIR, the main MHC-specific inhibitory receptors responsible for self versus non self recognition. Previously, it has been shown that only cells expressing self-MHC specific KIRs are responsive to activating stimuli. In this study, it was demonstrated that induction of self-MHC specific KIR by cytokines leads to acquisition of functional competence. Ex vivo analysis of human tissues suggests that acquisition of KIR and consequently of cytotoxic competence may occur in inflamed SLO. Finally, it was demonstrated that CD56dim NK cells do not represent a homogenous population. When dissected for CD62L and KIR expression, a new subset of NK cells could be identified, namely CD56dimCD62L+, which uniquely combines properties of CD56br NK cells, particularly high IFN-g production upon cytokine stimulation, proliferation and potential to migrate into SLO, with the capacity of CD56dim to kill, produce cytokines upon activating receptor stimulation and to migrate into inflamed tissues. Ex vivo analysis of the function, phenotype, telomere length and frequencies during ageing of CD56br, CD56dimCD62L+ and CD56dimCD62L- NK cells suggest that CD56dimCD62L+ cells represent an intermediate stage of NK cell maturation between the more immature CD56br and the terminally differentiated CD56dim CD62L- NK cells.
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Saint-Georges, Stéphane. "Leucémie lymphoïde chronique et microenvironnement : stimulation du récepteur B à l'antigène et régulation de l'expression membranaire du CXCR4 par les protéines kinases D." Paris 13, 2013. http://scbd-sto.univ-paris13.fr/secure/edgalilee_th_2013_saint_georges.pdf.
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L’évolutivité de la Leucémie Lymphoïde Chronique (LLC) se caractérise par la présence d’adénopathie résultant d’une accumulation de lymphocytes B (LB) pathologiques au sein du microenvironnement ganglionnaire. La stimulation antigénique joue un rôle important dans le trafic intra-ganglionnaire des LB suggérant qu’elle puisse jouer un rôle dans la rétention/accumulation des LB pathologiques au sein des ganglions. Dans ce contexte nous avons étudié l’impact in vitro de la stimulation antigénique des cellules de LLC sur l’expression d’effecteurs clés du trafic ganglionnaire des LB. Nous avons d’abord montré que la stimulation du récepteur B à l’antigène (BCR) entraine une diminution de l’expression membranaire du CXCR4 et du CD62L associée à une diminution de la migration et de l’adhésion in vitro des LB de LLC. De plus, l’intensité de la down-régulation du CXCR4 et du CD62L en réponse à la stimulation du BCR est associée à des marqueurs de mauvais pronostique et corrélé à la survie sans progression des patients LLC. Nous avons ensuite analysé les voies de signalisation activées en aval du BCR et impliquées dans l’internalisation du CXCR4 dans les LB de LLC. L’utilisation d’inhibiteurs de la PI3K (LY294002, CAL101) et des protéines kinases D (Gö6976, CID755673) entraîne une inhibition complète de la down-régulation du CXCR4 dépendante de la stimulation du BCR, révélant un rôle de ces kinases dans ce processus. D’un point de vue fonctionnel, la stimulation du BCR induit une phosphorylation/activation des PKD2 et/ou PKD3 de manière dépendante de la PI3K et le taux d’induction de la phosphorylation des PKD2/3 est corrélé à l’intensité de downrégulation du CXCR4. Enfin, l’activation du BCR induit une phosphorylation du CXCR4 sur des résidus impliqués dans l’internalisation du récepteur, suggérant que ce processus d’endocytose est en partie placé sous le contrôle des PKD. En conclusion, nos résultats ont permis de mettre en évidence une implication de la PI3K et des PKD dans la down-régulation du CXCR4 membranaire en réponse à une activation du BCR. Ces données suggèrent que ces protéines pourraient jouer in vivo un rôle dans la perturbation du trafic ganglionnaire des LB de LLC en réponse à la stimulation antigéniqueChronic Lymphocytic Leukaemia (CLL) progression involves enlargement of lymph nodes due to an accumulation of CLL B cells into the nodal microenvironment. The crucial role of the antigenic stimulation through the B cell receptor (BCR) in normal B cell trafficking into the lymph nodes suggests that BCR engagement might be implicated in the CLL B cell retention/accumulation into the lymphatic compartment. In this context, we focused our efforts on the study of the impact of an in vitro antigenic stimulation on the expression of key effectors involved in CLL B trafficking. First, we demonstrated that BCR stimulation decreased CXCR4- and CD62L-membrane expressions; this decrease was associated to an in vitro reduction of CLL B cell migration and adhesion. Moreover, the intensity of CXCR4- and CD62L- down-regulation upon BCR stimulation was linked to unfavourable prognostic markers and correlated to CLL patients’ progression free survival. Next, we analysed the activated BCR signalling cascades that were involved in CXCR4 internalization of CLL B cells. The LY294002/CAL101-PI3K and Gö6976/CID755673-PKD inhibitors blocked BCR-dependent CXCR4 down-regulation, revealing the role of the PKDs in this process. Functionally, BCR triggering induced PKD2/3 phosphorylation/activation in a PI3K-dependent manner. Interestingly, the level of the phospho-PKD2/3 induction was correlated to the intensity of BCR-dependent CXCR4 down-regulation. Furthermore, BCR engagement allowed CXCR4 phosphorylation on specific residues involved in its internalization, suggesting that CXCR4 endocytic process was partially regulated by PKDs. Altogether, our results demonstrated the PI3K and PKD implications on cell surface CXCR4 downregulation in response to BCR stimulation. These data proposed that PI3K and PKDs could play a role in the altered lymphatic trafficking of CLL B cells upon BCR engagement
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Sousa, Daniel Willian Lustosa de. "ExpressÃo da L-Selectina e do CD44 nas leucemias linfÃides agudas em crianÃas e dolescentes." Universidade Federal do CearÃ, 2009. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=8756.
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IntroduÃÃo â AlteraÃÃes na expressÃo ou funÃÃo das molÃculas de adesÃo (MA) nas cÃlulas leucÃmicas podem contribuir para a evoluÃÃo e no comportamento biolÃgico das leucemias agudas. A expressÃo aumentada nas LLAs parece relacionar-se aos mecanismos de disseminaÃÃo extramedular dos linfoblastos, infiltraÃÃo do SNC e formaÃÃo de massas tumorais. Objetivos â Analisar a expressÃo da L-selectina e do CD44 nas LLAs em crianÃas e adolescentes. Avaliar os fatores prognÃsticos (idade, sexo, leucometria ao diagnÃstico, imunofenÃtipo, classificaÃÃo FAB, EGIL, Ãndice de DNA e resposta ao tratamento de induÃÃo) e as apresentaÃÃes extramedulares das LLAs e correlacionÃ-los com essas MA. Pacientes e MÃtodos â Foram avaliados 76 pacientes com LLA, tratados com o Protocolo GBTLI-LLA. O diagnÃstico foi baseado em critÃrios FAB, imunofenotÃpicos (EGIL) e citogenÃticos. A expressÃo das MA foi avaliada por citometria de fluxo, utilizando tripla marcaÃÃo. O anticorpo monoclonal CD45-PerCP (ImmunotechÂ) foi utlizado como marcador dos linfoblastos. O CD44-PE (Clone HP2/9 - ImmunostepÂ) e o CD62L-FITC (Clone HI62L - ImmunostepÂ) foram utilizados para a marcaÃÃo das MA. Para a anÃlise das amostras e o cÃlculo da intensidade mÃdia de fluorescÃncia foi utilizado o programa Cell Quest. Na anÃlise estatÃstica utilizou-se o software SPSS 16.0. A associaÃÃo entre as variÃveis, os fatores prognÃsticos e resposta foi realizada com os testes de Qui-quadrado, exato de Fisher e Mann-Whitney. Sobrevida global foi determinada por curvas Kaplan-Meier e teste log-rank. AnÃlise multivariada por modelo proporcional de Cox foi utilizada para assegurar a independÃncia dos fatores prognÃsticos. Resultados â A mÃdia de idade foi 6,3Â0,5 anos (5m -17a) e predominou o sexo masculino (65%). Ao diagnÃstico os achados clÃnicos foram: hepatomegalia (63%), esplenomegalia (58%) e linfadenomegalia (44%). A infiltraÃÃo SNC ocorreu em 6,6% dos casos e o alargamento de mediastino em 11,8%. Quanto ao risco, 54% eram baixo risco e 46% alto risco. A classificaÃÃo FAB determinou 83% como L1 e 17% L2. DiagnÃstico de LLA-B foi mais frequente (89,5%) e o da LLA-T em 10,5% dos pacientes. O subtipo EGIL mais prevalente foi B II e B III, 51,5% e 45% respectivamente. O IDNA ≥ 1.16 foi encontrado em 19% dos pacientes e associou-se a bom prognÃstico. Na avaliaÃÃo do D8, 95% dos pacientes apresentaram contagem de blastos <1000/mm3 e leucÃcitos < 5.000/mm3. A taxa de remissÃo de induÃÃo foi de 95% e ocorreram 2,6% de Ãbitos na induÃÃo. Observou-se uma maior expressÃo do CD44 na LLA-T (87,5%/ IMF=150,44Â20,29), porÃm sem significÃncia estatÃstica. LLAs com massa tumoral apresentaram 84% de expressÃo do CD44, quando comparada a 52% das LLAs sem massa tumoral (p=0.01; OR=4,8). ExpressÃo aumentada da L-selectina na LLA-T (87,5%/IMF=272,33Â52,72) foi estatisticamente significante (p=0,004), comparado a LLA-B (54,5%/ IMF= 115,90Â12,75). NÃo houve correlaÃÃo entre os outros fatores prognÃsticos e essas MA. Na anÃlise multivariada as variÃveis de maior impacto para a sobrevida foram: a leucometria ao diagnÃstico, sexo, imunofenÃtipo T e a L-selectina. ConclusÃo â A expressÃo da L-selectina e do CD44 estÃo aumentadas nas LLAs estudadas, principalmente na LLA-T. O CD44 correlacionou-se com LLAs com massas tumorais e parece estar relacionado aos mecanismos de disseminaÃÃo extramedular dos linfoblastosIntroduction â Altered expression or function of adhesion molecules on leukemic blasts may contribute to the evolution of acute leukemia and its biological behavior. The elevated expression of adhesion molecules in ALL might be correlated with the extramedullary dissemination of blast cells, CNS involvement and leukemia tumor burden. Purpose â To analyze the expression of L-selectin and CD44 in ALL in children and adolescents. As well as to evaluate the prognostic factors (age, gender, initial leukocyte count, immunophenotype, FAB and EGIL classification, DNA index and early response to treatment) and the extramedullary presentation of ALL, to finally correlate the prognostic factors with these adhesion molecules. Patients and Methods â From November 2007 to November 2008, 76 patients with newly diagnosed ALL started on Brazilian GBTLI-ALL Protocol. The diagnosis was based on cytological, immunophenotypic, and cytogenetic methods. The mean fluorescence intensity (MFI) and the percentage of the adhesion molecules blasts cells was measured by flow cytometry using triple staining with McAb directly conjugated. CD45-PerCP positive cells were gated for blasts analysis. Anti-CD44-PE (Clone HP2/9 - ImmunostepÂ) and CD62L-FITC (Clone HI62L - ImmunostepÂ) were used to mark the adhesion molecules. The Cell Quest program was used for data acquisition and analysis. Statistical analysis was done by SPSS 16.0 Software. The association of features, prognosis and response to treatment was assessed by Chi-square, Fisher exact and Mann-Whitney tests. Overall survival curves were constructed by the Kaplan-Meier method and the log-rank test. Multivariate Cox regression analysis showed independent prognostic factors. Results â The mean age at diagnosis was 6.3Â0.5 years (range 9mo to 17yr) and 65% of them were boys. Clinical findings were hepatomegaly (63%), splenomegaly (58%), lymphadenopathy (44%). CNS involvement was detected in 6.6% of cases and mediastinal mass appeared in 11.8% of them. Patients were classified into low risk (54%) and high risk (46%). FAB classification identified 83% as L1 and 17% as L2. Immunophenotypically, 89.5% of patients were classified as B-lineage ALL and 10.5% as T-lineage ALL. The most frequent EGIL subtype was B common and pre-B-ALL (51.5% and 45.5%, respectively). DNA index greater than 1.16 was found in 19% of the patients and was associated with favorable prognosis. On the D8 evaluation, 95% of the patients had blast count lower than 1.000/mm3 and leukocyte count lower than 5.000/mm3. The remission induction rate was 95% and there was a rate of 2.6% of death during induction therapy. CD44 had greater expression to the rate of 87.5% in T-cell ALL (MFI=150.44Â20.29) with no statistical correlation. A significant positive correlation was demonstrated between 84% of CD44 expression and Leukemia burden tumor cases (p=0.01; OR=4.8). There was statistical correlation between L-selectin expression (87.5%/MFI=272.33Â52.72) and T-cell ALL (p=0,004). No significant correlation was detected between L-selectin and CD44 expression and other prognostic factors. Multivariate statistical analysis (adjusted for overall survival) indicated that initial leukocyte count, gender, T immunophenotype and L-selectin were independent factors. Conclusion â L-selectin and CD44 expressions were elevated in ALL studied, mainly in T-cell ALL. The research demonstrated that there is an association between CD44 expression and leukemia tumor burden, which might be involved in the dissemination of leukemic cells and the progression of the disease.
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Faulhaber, Fabrízia Rennó Sodero. "Expressão de marcadores de superfície de neutrófilos em recém nascidos ictéricos antes e após a fototerapia." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/179819.
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A icterícia por hiperbilirrubinemia indireta afeta mais de 60% dos recém-nascidos a termo. O tratamento, quando necessário, é realizado através da fototerapia. Não existem estudos na literatura avaliando os efeitos da fototerapia na função dos neutrófilos de recém-nascidos. O melhor entendimento da função dos neutrófilos nos recém-nascidos antes e após a fototerapia seria importante para avaliar as possíveis repercussões na expressão dos neutrófilos desencadeadas pelo tratamento fototerápico. O objetivo deste estudo foi avaliar e comparar a função dos neutrófilos, através da mensuração pela citometria de fluxo da expressão dos principais marcadores de superfície em recémnascidos ictéricos, antes e após 24 horas de fototerapia. Metodologia: Foram incluídos recém-nascidos com idade gestacional ≥ 35 semanas e peso de nascimento ≥ 2000g, que possuiam critérios da Academia Americana de Pediatria para tratamento fototerápico. Os critérios de exclusão foram: mal-formações congênitas, síndromes com alterações cromossômicas, erro inato do metabolismo, infecções do grupo STORCH, asfixia neonatal, sepse ou suspeita de sepse, exsanguineotransfusão, transfusão de hemocomponentes e uso de imunoglobulina. Foi realizada a avaliação de expressão da intensidade média de fluorescência (IMF) de CD10, CD11b, CD11c, CD15, CD16, CD18, CD62L, CD64 e CD66, antes do início e após 24 horas do início da fototerapia. Foram utilizados o teste T de Student para análise dos dados. Resultados: Foram incluídos 25 recém-nascidos no estudo, com idade mediana de 53 (27.5-75.5) horas de vida e bilirrubina média de 13.6±2.85 mg/dL. Não houve diferença estatística na expressão de CD11b, CD15, CD18, CD62L, CD64 e percentual de neutrófilos antes e após 24 horas de fototerapia. Ocorreu aumento da expressão de CD10 8 (p=0.038) e CD16 (p=0.017) e redução da expressão de CD11c (p=0.023) e CD66acde (p=0.004) após 24 horas de fototerapia. Conclusão: Os recém-nascidos submetidos ao tratamento fototerápico apresentaram aumento da expressão de CD10 e de CD16 e diminuição da expressão de CD11c e de CD66acde após 24 horas de exposição, que pode estar relacionado a um efeito antiinflamatório da fototerapia nos recém-nascidos expostos a este tratamento.Jaundice due to indirect hyperbilirubinemia affects more than 60% of term neonates. The treatment when necessary is carried out using phototherapy. There are no studies in the literature evaluating the effect of phototherapy on the function of neonates' neutrophils. A better understanding of the function of neutrophils in neonates before and after phototherapy would be important in order to assess potential effects on the expression of neutrofils triggered by the phototherapy treatment. The aim of this study was to assess and compare the function of neutrophils by measuring the expression of the main surface markers in icteric neonates, using flow cytometry, before and after 24 hours of phototherapy. Methodology: Neonates at a gestational age ≥ 35 weeks and at a birth weight ≥ 2000g who met the criteria of the American Academy of Pediatrics for phototherapy were included. The exclusion criteria were: congenital malformations, syndromes with chromosomal alterations, inborn errors of metabolism, infections of the STORCH group, neonatal asphyxia, sepsis or suspicion of sepsis, exchange transfusion, transfusion of blood components, and use of immunoglobulin. The evaluation of the MFI expression of CD10, CD11b, CD11c, CD15, CD16, CD18, CD62L, CD64 and CD66 was performed before and 24 hours after the initiation of phototherapy. The chi-square and Student T tests were used for data analysis. Results: Twenty-five neonates were included in the study at the mean age of 53 (27.5- 75.5) hours of life and with a mean bilirubin level of 13.6±2.85 mg/dL. There was no statistical difference in the expression of CD11b, CD15, CD18, CD62L, CD64 and percentage of neutrophils before and after 24 hours of phototherapy. There was an increase in the expression of CD10 (p=0.038) and CD16 (p=0.017) and a reduction in 10 the expression of CD11c (p=0.023) and CD66acde (p=0.004) after 24 hours of phototherapy. Conclusion: The newborns submitted to phototherapy had increased expression of CD10 and CD16 and decreased expression of CD11c and CD66acde after 24 hours of exposure, which may be related to an anti-inflammatory effect of phototherapy on the neonates exposed to this treatment.
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Malaud, Éric. "Étude structurale et fonctionnelle de deux molécules d'adhésion (CD62P et CD36) dans l'initiation et le développement des lésions athéromateuses." Lyon 1, 2001. http://www.theses.fr/2001LYO1T061.
Full textBook chapters on the topic "CD62L"
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Gupta, G. S. "L-Selectin (CD62L) and Its Ligands." In Animal Lectins: Form, Function and Clinical Applications, 553–74. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-1065-2_26.
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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "Cdc2l." In Encyclopedia of Signaling Molecules, 364. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100222.
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Gutensohn, K., J. Riggert, C. Asmussen, A. Alisch, and P. Kuehnl. "P-selectin (CD62p) and Soluble CD62p (sCD62p) in Platelet Concentrates Stored for Transfusion." In 27. Hämophilie-Symposion Hamburg 1996, 252–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80403-8_36.
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Gupta, G. S. "E-Selectin (CD62E) and Associated Adhesion Molecules." In Animal Lectins: Form, Function and Clinical Applications, 593–616. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-1065-2_28.
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Lindenblatt, Nicole, W. Schareck, L. Belusa, R. M. Nickels, M. D. Menger, and B. Vollmar. "Antioxidatives Ebselen inhibiert die thrombozytäre CD62P-Expression und wirkt anti-thrombogen in vivo." In Deutsche Gesellschaft für Chirurgie, 485–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-19024-7_134.
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Lindenblatt, N., W. Schareck, L. Beiusa, R. M. Nickels, M. D. Menger, and B. Vollmar. "Antioxidatives Ebselen inhibiert die thrombozytäre CD62P-Expression und wirkt anti-thrombogen in vivo." In Zurück in die Zukunft, 459–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55611-1_279.
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Barclay, A. Neil, Marion H. Brown, S. K. Alex Law, Andrew J. McKnight, Michael G. Tomlinson, and P. Anton van der Merwe. "CD62L." In The Leucocyte Antigen FactsBook, 298–300. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012078185-0/50502-3.
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"CD62 Antigen-Like Family Member E (CD62E)." In Encyclopedia of Cancer, 854. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_100456.
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"Cdc2l." In Encyclopedia of Signaling Molecules, 975. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_100670.
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Barclay, A. Neil, Marion H. Brown, S. K. Alex Law, Andrew J. McKnight, Michael G. Tomlinson, and P. Anton van der Merwe. "CD62E." In The Leucocyte Antigen FactsBook, 295–97. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012078185-0/50501-1.
Full textConference papers on the topic "CD62L"
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Lins, Lucas Costa, Iana Carneiro Pinto, Nathalia Lima Schramm dos Santos, Vitor de Oliveira Silva, and Marcos Lázaro da Silva Guerreiro. "INFLUÊNCIA DA QUIMIOTERAPIA NA RESPOSTA IMUNOLÓGICA CELULAR EM CAMUNDONGOS INFECTADOS COM AS CEPAS Y E COLOMBIANA DO TRYPANOSOMA CRUZI." In I Congresso Brasileiro de Parasitologia Humana On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/741.
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Introdução: Estudos sugerem que o tratamento quimioterápico estimula o sistema imunológico em camundongos infectados com cepas do T. cruzi. Objetivo: avaliar a influência do tratamento com Benzonidazol sobre a resposta imunológica celular em camundongos infectados com a cepa Y (suscetível) e Colombiana (resistente). Material e métodos: 150 camundongos, subdivididos em: Infectados tratados cepa Y (YT) e não tratados (Y-NT); Colombiana tratados (COL-T) e não tratados (COL-NT), Tratados não infectados (TNI) e Controles sem tratamento (CI). O inóculo foi 1,0 x 104 por via intraperitoneal. Os procedimentos estiveram de acordo ao protocolo CEUA, 013/09. O tratamento foi iniciado no pico parasitêmico das cepas, sendo no 7º dia após a infecção nos infectados pela cepa Y e, nos tratados e não infectados, no 18º nos infectados pela cepa Colombiana. A quimioterapia foi em 60 doses (100mg/kg/dia). Os camundongos eutanasiados na fase aguda e crônica nos grupos tiveram a resposta celular investigada pelas citocinas IL-6 IL-10, MCP-1, INF-γ e TNF-α e pelas subpopulações celulares no baço de CD4+ , CD8+ , células de memórias CD62L, células B e macrófagos. Resultados: as citocinas circulantes IL-6 IL-10, MCP-1, INF-γ e TNF-α, foram mais elevadas nos animais infectados com a cepa Y, o tratamento com Benz, não alterou os índices circulantes nos TNI. A citometria na fase aguda demonstrou maior frequência de CD4+ e CD8+ no grupo TNI; de células de memória (CD62L/CD4 e CD8) no grupo YT; de CD11b no grupo COL-NT fase aguda e na YT na fase crônica; e de células B (B220) no grupo CI. Na fase crônica maior frequência de CD4+ e CD8+ no grupo COL-T; de células de memória: (CD4/CD62L) no grupo YT e (CD8/CD62L) no COL-T; de CD11b no YT; e de células B (B220) CI. Conclusão: Nossos resultados sugerem que o tratamento com Benz tem influência na resposta imunológica celular em camundongos.
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Makiyah, Sri Nabawiyati Nurul, Widodo, Muhaimin Rifa’i, and Muhamad Sasmito Djati. "The influence of ethanol extract Dioscorea alata L. on CD4+CD62L+ and CD8+CD62L+ profile of BALB/c mice model digestive tract allergy." In TOWARDS THE SUSTAINABLE USE OF BIODIVERSITY IN A CHANGING ENVIRONMENT: FROM BASIC TO APPLIED RESEARCH: Proceeding of the 4th International Conference on Biological Science. Author(s), 2016. http://dx.doi.org/10.1063/1.4953528.
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Cane, JL, SHR Waite, and M. Bafadhel. "S14 Eosinophil activation status and CD62L expression in airways disease." In British Thoracic Society Winter Meeting 2018, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 5 to 7 December 2018, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2018. http://dx.doi.org/10.1136/thorax-2018-212555.20.
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Suzuki, Shoji, Makoto Ishii, Takanori Asakura, Ho Namkoong, Satoshi Okamori, Kazuma Yagi, Hirofumi Kamata, et al. "ADAM17 protects mice against elastase-induced emphysema via inactivation of CD62L." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4267.
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Lokwani, Ravi, Peter Wark, Katherine Baines, Daniel Barker, Michael Fricker, and Jodie Simpson. "Circulatory neutrophils in COPD feature downregulated CD62L expression in comparison with asthma and healthy participants." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4384.
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Singh, Nanak R., Charlotte Summers, Andrew Johnston, Adrien M. Peters, and Edwin R. Chilvers. "Differential Effects Of Sepsis And Acute Respiratory Distress Syndrome (ARDS) On CD62L Expression In Neutrophils Entering And Leaving The Lung." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1037.
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Choudhary, Dharamainder, Poornima Hegde, Shilpa Choudhary, Kevin Claffey, Pramod Srivastava, Carol C. Pilbeam, and John Arthur Taylor. "Abstract 53: Increased expression of L-selectin (CD62L) in high grade bladder cancer: a potential biomarker for lymph node metastasis." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-53.
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Lange, Christian M., Thuy Y. Tran, Harald Farnik, Sven Jungblut, Thomas O. Wagner, and Tim O. Hirche. "Increased Frequency Of Regulatory T-Cells And Selection Of Highly Potent CD62L+ Cells During Treatment Of Human Lung Recipients With Rapamycin." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2575.
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Alzua, Brian, Mark Smith, and Yan Chen. "A Flow Cytometry Method for Characterizing Platelet Activation." In 2020 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/dmd2020-9070.
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Abstract Hemocompatibility testing is critical for assessing the safety of blood-contacting medical devices. Comprehensive hemocompatibility testing requires examining a wide range of possible adverse effects cause by direct or indirect blood contact, such as hemolysis, complement activation, and thrombus formation [1]. Moreover, these domains each encompass complex intercellular processes with many potential targets for analysis. For example, the current testing paradigm of platelet function may involve exposing the device to human whole blood and performing simple blood counts and/or macroscopic evaluation to determine the extent of platelet activation and clot formation as described in ASTM F2888-19. However, this approach does not capture any observations for device-mediated initiation of any steps in the platelet activation pathway prior to aggregation. We have validated a method to evaluate platelet activation by quantifying surface p-selectin expression after exposure to various materials. This method will provide an additional level of detail about potential platelet activating properties of a medical device. Flow cytometry has been used previously to measure platelet activation for clinical and research purposes. We sought to adapt this method to test for platelet activation induced by exposure of blood to medical devices or materials. We determined that processing fresh whole blood to platelet-rich plasma (PRP) by gentle centrifugation enhanced the signal compared to fresh blood itself. In each experiment, devices were exposed to PRP according to an extraction ratio of 6 cm2/mL for 1 hour. A blank control consisting of untreated PRP, and a positive control consisting of ADP, a potent agonist, were also used. After the exposure, excess plasma was removed from the articles and combined with anti-CD61 (to stain for platelets) and anti-CD62P (to stain for activated platelets) antibodies. Flow cytometry was then performed to quantify the percentage of CD62P+ over the total CD61+ cells to measure the percentage of activated platelets. In order to optimize the method, we investigated the effect of several experimental factors, including anticoagulant usage, donor variability, and selection of reference materials to serve as controls. Our results indicate that the flow cytometry-based method is consistent and reproducible, quick and easy to perform, and is well-correlated with results from the standard platelet and leukocyte count assay. The flow cytometry-based platelet activation method is a powerful supplement to the standard regimen of medical device hemocompatibility testing.