Готові списки джерел за темами / Lymphocyte activity

Добірка наукової літератури з теми "Lymphocyte activity"

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 29 січня 2023

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Статті в журналах з теми "Lymphocyte activity"

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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Nakhaei-Nejad, Maryam, Amer M. Hussain, Qiu-Xia Zhang, and Allan G. Murray. "Endothelial PI 3-kinase activity regulates lymphocyte diapedesis." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 6 (December 2007): H3608—H3616. http://dx.doi.org/10.1152/ajpheart.00321.2007.

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Lymphocyte recruitment to sites of inflammation involves a bidirectional series of cues between the endothelial cell (EC) and the leukocyte that culminate in lymphocyte migration into the tissue. Remodeling of the EC F-actin cytoskeleton has been observed after leukocyte adhesion, but the signals to the EC remain poorly defined. We studied the dependence of peripheral blood lymphocyte transendothelial migration (TEM) through an EC monolayer in vitro on EC phosphatidylinositol 3-kinase (PI 3-kinase) activity. Lymphocytes were perfused over cytokine-activated EC using a parallel-plate laminar flow chamber. Inhibition of EC PI 3-kinase activity using LY-294002 or wortmannin decreased lymphocyte TEM (48 ± 6 or 34 ± 7%, respectively, vs. control; mean ± SE; P < 0.05). Similarly, EC knockdown of the p85α regulatory subunit of PI 3-kinase decreased lymphocyte transmigration. Treatment of EC with jasplakinolide to inhibit EC F-actin remodeling also decreased lymphocyte TEM to 24 ± 10% vs. control ( P < 0.05). EC PI 3-kinase inhibition did not change the strength of lymphocyte adhesion to the EC or formation of the EC “docking structure” after intercellular adhesion molecule-1 ligation, whereas this was inhibited by jasplakinolide treatment. A similar fraction of lymphocytes migrated on control or LY-294002-treated EC and localized to interendothelial junctions. However, lymphocytes failed to extend processes below the level of vascular endothelial (VE)-cadherin on LY-294002-treated EC. Together these observations indicate that EC PI 3-kinase activity and F-actin remodeling are required during lymphocyte diapedesis and identify a PI 3-kinase-dependent step following initial separation of the VE-cadherin barrier.

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Compaan, Deanne M., Lino C. Gonzalez, Irene Tom, Kelly M. Loyet, Dan Eaton, and Sarah G. Hymowitz. "Attenuating Lymphocyte Activity." Journal of Biological Chemistry 280, no. 47 (September 16, 2005): 39553–61. http://dx.doi.org/10.1074/jbc.m507629200.

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Dallegri, F., F. Patrone, G. Frumento, A. Ballestrero, and C. Sacchetti. "Down-regulation of K cell activity by neutrophils." Blood 65, no. 3 (March 1, 1985): 571–77. http://dx.doi.org/10.1182/blood.v65.3.571.571.

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Abstract Human neutrophils, activated by phorbol-myristate acetate (PMA), (A- neutrophils), were found to suppress lymphocytic killer (K) cell- mediated antibody-dependent cellular cytotoxicity (ADCC). Resting (R) neutrophils, ie, PMA-untreated cells, were completely ineffective. Suppression was optimal when A-neutrophils were added at the beginning of the ADCC assay. Furthermore, A-neutrophils were found to cause an approximately 80% reduction in the number of Raji target cell-bound lymphocytes. These data indicate that A-neutrophils inhibit K cell activity by interfering with the target cell recognition. A-neutrophils were capable of reducing the percentage of Fc receptor (FcR)-bearing lymphocytes with a half-time of 7.2 minutes, through a process preventable by the serine-protease inhibitors tosyl-lysine-chloromethyl ketone (TLCK) and lima bean trypsin inhibitor (LBTI). Conversely, A- neutrophils caused a very slow decrease in the amount of Raji cell- bound antibodies, as detected by the complement-mediated lytic assay. Thus, only lymphocyte FcR structures seem to be highly susceptible to neutrophil-derived TLCK- and LBTI-inhibitable proteases. Furthermore, supernatants from A-neutrophils were found to inhibit K cell ADCC and lymphocyte binding to Raji target cells. In addition, LBTI prevented the A-neutrophil-dependent and the supernatant-dependent inhibition of both K cell ADCC activity and lymphocyte-target cell conjugate formation. Together these data suggest that A-neutrophils suppress K cell function through a protease-mediated impairment of the FcR binding capacity. The results provide evidence that human neutrophils are endowed with mechanisms to regulate K cell ADCC activity.

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Human neutrophils, activated by phorbol-myristate acetate (PMA), (A- neutrophils), were found to suppress lymphocytic killer (K) cell- mediated antibody-dependent cellular cytotoxicity (ADCC). Resting (R) neutrophils, ie, PMA-untreated cells, were completely ineffective. Suppression was optimal when A-neutrophils were added at the beginning of the ADCC assay. Furthermore, A-neutrophils were found to cause an approximately 80% reduction in the number of Raji target cell-bound lymphocytes. These data indicate that A-neutrophils inhibit K cell activity by interfering with the target cell recognition. A-neutrophils were capable of reducing the percentage of Fc receptor (FcR)-bearing lymphocytes with a half-time of 7.2 minutes, through a process preventable by the serine-protease inhibitors tosyl-lysine-chloromethyl ketone (TLCK) and lima bean trypsin inhibitor (LBTI). Conversely, A- neutrophils caused a very slow decrease in the amount of Raji cell- bound antibodies, as detected by the complement-mediated lytic assay. Thus, only lymphocyte FcR structures seem to be highly susceptible to neutrophil-derived TLCK- and LBTI-inhibitable proteases. Furthermore, supernatants from A-neutrophils were found to inhibit K cell ADCC and lymphocyte binding to Raji target cells. In addition, LBTI prevented the A-neutrophil-dependent and the supernatant-dependent inhibition of both K cell ADCC activity and lymphocyte-target cell conjugate formation. Together these data suggest that A-neutrophils suppress K cell function through a protease-mediated impairment of the FcR binding capacity. The results provide evidence that human neutrophils are endowed with mechanisms to regulate K cell ADCC activity.

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Beno, D. W., A. G. Stöver, and H. L. Mathews. "Growth inhibition of Candida albicans hyphae by CD8+ lymphocytes." Journal of Immunology 154, no. 10 (May 15, 1995): 5273–81. http://dx.doi.org/10.4049/jimmunol.154.10.5273.

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Abstract We have shown previously that IL-2-activated splenocytes can inhibit the growth of Candida albicans hyphae in vitro. Herein we demonstrate that plastic nonadherent lymphocytes that are CD8+ mediate the antifungal activity. Enrichment for CD8+ cells markedly enhanced the antifungal activity of the IL-2-activated lymphocyte population for C. albicans and the cytotoxic activity of the lymphocytes for an NK-resistant cell line. Depletion of CD8+ cells reduced the lymphocyte population's antifungal activity and cytotoxic activity for the NK-resistant cell line. Enrichment for NK1.1+ cells markedly reduced the antifungal activity of the lymphocyte population for C. albicans and increased the cytotoxic activity of the lymphocytes for an NK-sensitive cell line. Depletion of NK1.1+ cells increased the lymphocyte population's antifungal activity and cytotoxic activity for the NK-resistant cell line. Generation of the antifungal lymphocytes in culture required IL-2 and was not replaced with IFN-gamma. These data show that IL-2-activated CD8+ T lymphocytes exert the greatest amount of antifungal effect against the hyphal form of C. albicans, whereas IL-2- or IFN-gamma-activated NK cells have little or no effect against the hyphae.

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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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Feldman, L., and N. Dainiak. "B-lymphocyte-derived erythroid burst-promoting activity is distinct from other known lymphokines." Blood 73, no. 7 (May 15, 1989): 1814–20. http://dx.doi.org/10.1182/blood.v73.7.1814.1814.

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Abstract Previously we have demonstrated that, in contrast to various panspecific or multilineage hematopoietic growth factors, lymphocyte- derived erythroid burst-promoting activity (BPA) is lineage specific, stimulating BFU-E proliferation in serum-free culture by up to 600% of control values while failing to enhance nonerythroid colony formation. To further determine the cellular source(s) of this important erythropoietic growth regulator, we have separated normal nonadherent peripheral blood and splenic lymphocytes by nylon wool fractionation, SRBC rosetting, and panning with monoclonal antibodies (MoAbs). These unstimulated T- and B-lymphocyte-enriched populations were used as cell sources to produce conditioned media (CM) and to prepare plasma membranes (PM). When CM fractions or purified PM were assayed in serum- free human bone marrow culture, BPA was localized entirely to the B- lymphocyte-derived fractions. While CM or PM from unstimulated T lymphocytes failed to stimulate BFU-E proliferation, activation of T cells by either phytohemagglutinin-M (1%) or concanavalin A (Con A; 5 micrograms/mL) induced the expression of a factor on the PM and in the resultant CM that stimulated the formation of erythroid bursts. In addition to enhancing BFU-E proliferation, this T-cell factor stimulated the proliferation of CFU-GM and CFU-GEMM in serum-free culture. When compared biochemically (in terms of temperature stability, localization by ammonium sulfate fractionation, and sensitivity to dithiothreitol) or immunochemically (using antibodies specific for lymphocyte-derived BPA, GM-CSF, or interleukin-3 [IL-3]), as well as by lineage specificity, B- and activated T-lymphocyte- derived growth factors appeared to be distinct. The burst stimulatory activities expressed by recombinant human GM-CSF and IL-3 were immunologically distinct from that associated with octylglucoside extracts of plasma membranes from resting B lymphocytes. Our results suggest that the BFU-E-directed growth-promoting activity released from activated T lymphocytes is apparently due to GM-CSF, while both resting and mitogen-stimulated normal B lymphocytes express erythroid-specific BPA and neither GM-CSF nor IL-3.

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Previously we have demonstrated that, in contrast to various panspecific or multilineage hematopoietic growth factors, lymphocyte- derived erythroid burst-promoting activity (BPA) is lineage specific, stimulating BFU-E proliferation in serum-free culture by up to 600% of control values while failing to enhance nonerythroid colony formation. To further determine the cellular source(s) of this important erythropoietic growth regulator, we have separated normal nonadherent peripheral blood and splenic lymphocytes by nylon wool fractionation, SRBC rosetting, and panning with monoclonal antibodies (MoAbs). These unstimulated T- and B-lymphocyte-enriched populations were used as cell sources to produce conditioned media (CM) and to prepare plasma membranes (PM). When CM fractions or purified PM were assayed in serum- free human bone marrow culture, BPA was localized entirely to the B- lymphocyte-derived fractions. While CM or PM from unstimulated T lymphocytes failed to stimulate BFU-E proliferation, activation of T cells by either phytohemagglutinin-M (1%) or concanavalin A (Con A; 5 micrograms/mL) induced the expression of a factor on the PM and in the resultant CM that stimulated the formation of erythroid bursts. In addition to enhancing BFU-E proliferation, this T-cell factor stimulated the proliferation of CFU-GM and CFU-GEMM in serum-free culture. When compared biochemically (in terms of temperature stability, localization by ammonium sulfate fractionation, and sensitivity to dithiothreitol) or immunochemically (using antibodies specific for lymphocyte-derived BPA, GM-CSF, or interleukin-3 [IL-3]), as well as by lineage specificity, B- and activated T-lymphocyte- derived growth factors appeared to be distinct. The burst stimulatory activities expressed by recombinant human GM-CSF and IL-3 were immunologically distinct from that associated with octylglucoside extracts of plasma membranes from resting B lymphocytes. Our results suggest that the BFU-E-directed growth-promoting activity released from activated T lymphocytes is apparently due to GM-CSF, while both resting and mitogen-stimulated normal B lymphocytes express erythroid-specific BPA and neither GM-CSF nor IL-3.

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Robbins, R. A., S. Shoji, J. Linder, G. L. Gossman, L. A. Allington, L. W. Klassen, and S. I. Rennard. "Bronchial epithelial cells release chemotactic activity for lymphocytes." American Journal of Physiology-Lung Cellular and Molecular Physiology 257, no. 2 (August 1, 1989): L109—L115. http://dx.doi.org/10.1152/ajplung.1989.257.2.l109.

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Lymphocytes can frequently be observed in association with bronchial tissues. One mechanism that might account for this association is that bronchial epithelial cells might release chemotactic factors for lymphocytes. To test this hypothesis, bovine bronchial epithelial cells were cultured in serum-free media, and the supernatant fluids were harvested and evaluated for lymphocyte chemotactic activity using a blind-well chamber technique. Media alone attracted few lymphocytes (12 +/- 2 cells/high power field), but in contrast, there was a significant increase in the number of cells attracted by supernatant fluids obtained from bronchial epithelial cell cultures (40 +/- 6 cells/high power field, P = 0.002). The activity was dose dependent and was demonstrated to be chemotactic activity by checkerboard analysis. Partial characterization of the activity revealed it was not extractable into ethyl acetate but was partially inactivated by trypsin and heat (100 degrees C, 15 min). The responding cells were predominantly T-helper lymphocytes as shown by monoclonal antibody staining, with a smaller proportion being B-lymphocytes. Molecular sieve column chromatography revealed multiple peaks of lymphocyte chemotactic activity, with three of the peaks preferentially attracting T-helper lymphocytes and one of the peaks preferentially attracting B-lymphocytes. These data demonstrate that bronchial epithelial cells can release chemotactic factors for lymphocytes and suggest that bronchial epithelial cells may modulate their local population of immune effector cells.

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Більше джерел

Дисертації з теми "Lymphocyte activity"

Chu, Nelson Randall. "Characterization of a T lymphocyte-derived, antigen-binding molecule with suppressive activity." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/30608.

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Regulation of the immune response is mediated, in part, by the action of suppressor T cells (Ts). One intriguing aspect of these cells is the description of T cell suppressor factor (TsF): a soluble analog of the cell that shares many of its properties, such as the ability to bind free antigen (Ag) and suppress an Ag-specific immune response. The exact molecular nature of TsF and the relationship of TsF to Ts are unknown. The immune response to the small, bacterial protein, ferredoxin (Fd), was used as a model system to study TsF. A Fd-specific suppressor cell network has been described in mice that are genetically nonresponsive to this Ag. Previously, a soluble mediator, known as Fd11F, was found in the culture supernatant (SN) of the Ts hybridoma, Fd11. Fd11F possessed both Ag-binding activity and the ability to suppress the anti-Fd Ab response in mice. The TsF-specific monoclonal antibody, B16G, was used for both the recovery of Fd11F-enriched material from SN and its detection by the enzyme-linked immunosorbent assay. ' Further immunochemical, biological, and biochemical characterization of Fd11F was done with emphasis on describing the Ag-binding properties of Fd11F. It was found that Fd11F bound to solid- and liquid-phase Fd, and demonstrated preferential binding to the carrier determinant of the Ag. A spleen cell culture assay was devised which showed that Fd11F suppressed Ab production in a concentration-dependent manner. Additional experiments suggested that the suppressive effect was Ag-specific. The identification of the Ag-binding molecule was attempted by the fractionation of Fd11F-enriched material using high performance gel filtration or preparative SDS-PAGE (run under non-reducing conditions). Using SDS-PAGE, a unique, single polypeptide of about 30k relative molecular mass (Mr) was identified as the Ag-binding moiety of Fd11F. The possible relationship of this moiety to other identified materials is discussed.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate

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Endicott, Roger A. "Immunoregulation of T-lymphocyte proliferative activity by alveolar macrophages from mice bearing Lewis lung carcinoma tumors." Virtual Press, 1986. http://liblink.bsu.edu/uhtbin/catkey/458971.

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The immune regulatory abilities of alveolar macrophages from C57B1/6 mice bearing a metastatic variant of Lewis lung carcinoma were determined. During early stages of tumor development, or before tumors metastasized to the lungs, alveolar macrophages did not affect or slightly enhanced T-lymphocyte proliferation; as tumor growth progressed, or following tumor metastasis, alveolar macrophages suppressed the T-cell response. Macrophage suppressor activity was probably not mediated by their production of PGE, since macrophages of tumor-bearing mice secreted less 2 PGE than did macrophages of normal mice. Normal alveolar 2 macrophages or macrophages preincubated in tumor cell supernatant for a short period stimulated T-cell blastogenesis and secreted PGE during in vitro culture. However, with 2 longer exposure to tumor cell supernatant, alveolar macrophages lost the capacity to augment T-cell proliferation and secreted less PGE 2.Ball State UniversityMuncie, IN 47306

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Glashoff, Richard Helmuth. "Characterisation of cytolytic CD4+ and suppresor CD8+ activity of T lymphocyte clones derived from tuberculous pleuritis." Doctoral thesis, University of Cape Town, 2000. http://hdl.handle.net/11427/3390.

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Kane, Kim Kartchener. "In Vitro Identification of the Effect of Serotonin on Lymphocyte DNA Synthesis and Natural Killer Cell Activity." DigitalCommons@USU, 1989. https://digitalcommons.usu.edu/etd/5863.

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The purpose of this study was to identify the effects of the neurotransmitter, serotonin (SE), on the immune function of peripheral blood mononuclear cells (PBMC) of normal, healthy subjects. This was done as a preliminary investigation to studies on the association of SE with immune changes in autistic subjects. The PBMC isolated from normal male subjects were treated with various concentrations of SE for 48 hrs. Their incubation in SE at a concentration of 10-3 M induced about a 35% decrease in DNA synthesis. However, incubation of the cells in lower concentrations (10-4 to 10-10) of SE produced no significant effect. The ability of natural killer (NK) cells to lyse K562 target cells was also examined after incubation with SE for 48 hrs. The NK activity was almost completely eliminated following incubation in 10-3M of SE, but the activity was not significantly decreased by exposure to lower concentrations of SE. The viability of PBMC was not altered following incubation with SE under identical conditions as those utilized in the NK assay. Preliminary analysis using a fluorescence-activated cell sorter (FACS) of monoclonal antibodies directed against Tll (total T cell), T4 (helper T cell), T8 (suppressor and cytotoxic T cells), B-cell and NK cell markers indicated that the suppressive effect exerted by SE could be attributed to a decrease in the density of these markers or receptors on the cell surface. These findings provide additional evidence for a possible link between neurotransmitters, specifically SE, and immune function.

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Zheng, Chengyun. "Genetic polymorphisms and natural killer cell activity in multiple myeloma /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-222-1.

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Adewusi, Iyabode Olukemi 1958. "The Eosinophil and Lysophospholipase Responses in Mice Infected with Trichinella spiralis: A Role for the Lymphocyte and Macrophage." Thesis, North Texas State University, 1986. https://digital.library.unt.edu/ark:/67531/metadc331042/.

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The relationship among eosinophils, lysophospholipase activity and the immune response in animals infected with Trichinella spiralis was studied using in vivo and in vitro techniques. In an in vivo experiment, anti-thymocyte serum (ATS) was administered to mice infected with T. spiralis and its effects on intestinal lysophospholipase (EC 3.1.1.5.) activity, peripheral blood, bone marrow and intestinal eosinophilia were measured in the same experimental animal. The ATS caused a significant temporally related suppression of both the tissue lysophospholipase response and eosinophilia, in all three compartments. These findings support the hypothesis that parasite-induced eosinophilia is the cause of the increased lysophospholipase activity of parasitized tissue and that the responses are thymus cell-dependent. In vitro experiments demonstrated that the eosinophil was the primary inflammatory cell source of lysophospholipase among eosinophils, neutrophils macrophages and lymphocytes. The role of other cells and antigen in the production of the enzyme by the eosinophil was also investigated in vitro• Results demonstrated that eosinophils cultured with both T. spiralis antigen and other leukocytes yielded enzyme activities significantly greater than eosinophils cultured alone or with only antigen. More specific experiments showed that T-lymphocytes were the cells responsible for influencing the eosinophils' lysophospholipase activity in the presence of antigen, and that their influence was enhanced by the presence of macrophages. These results suggested that increased lysophospholipase activity present in parasitized tissue was not only due to increased numbers of eosinophils infiltrating parasitized tissue but was also due to each eosinophil synthesizing more of the enzyme. The necessity for antigen and other cells suggests a role for cell cooperation in the production of the enzyme, specifically T-lymphocytes and macrophage interaction with the eosinophil. A lymphocyte soluble factor collected from sensitized lymphocytes stimulated with specific antigen or concanavalin A was found to enhance the eosinophil lysophospholipase activity when added to cultures of eosinophils plus other peritoneal cells. The soluble factor did not stimulate the lysophospholipase activity of pure cultures of eosinophils.

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Marcellon, Roselande. "Profiling patients with type 2 diabetes on the paradox idea: the underappreciated role of toll-like receptors in B lymphocyte activity." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12504.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Type 2 diabetes (T2D) is a growing concern in most developed countries and in the US. The disease is associated with increased risk for certain diseases such as cardiovascular disease, kidney disease, retinopathy, neuropathies, dementia and most types of cancers. Many studies have established an association between chronic inflammation and diabetes pathology. Part of the pathology of T2D involves a chronic state of inflammation in which the immune response is altered. Toll-like receptors (TLRs), specifically Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4), play critical roles in mediating inflammation. Past studies have looked at the role TLRs play, but have not characterized their combined effects or the influences of other covariates such as various clinical and immunological parameters. This study aimed to investigate the role of TLRs, specifically TLR2 and TLR4, in B lymphocytes and how this expression can be used to profile and characterize disease severity in patients with T2D. This study used a subset of patients (n=SO) enrolled in an IRB approved and industry sponsored study in the Ganley-Leal lab in the Section of Infectious Disease Laboratory at Boston University Department of Medicine. Patient data was obtained from medical records, a short questionnaire, and heparinized blood samples. Serum concentrations of High Mobility Group Protein 1 (Hmgbl) and Limulus Amebocyte Lysate (endotoxin) were measured along with B lymphocyte TLR expression and cellular responses to TLR ligands. Bivariate tests, tests for linear associations and an analysis of variance (ANOVA) were performed on clinical, immunologic and disease severity index parameters. The study found that TLR2 expression on B cells was both significantly associated and correlated positively with triglyceride levels. High basal IL-8 production was important in characterizing level of response for clinical parameters. The data suggests that IL-8 production and DSI score, in conjunction with TLR2 expression by B cells, can help profile patients with T2D and characterize additional risks that may be overlooked when using parameters like glycated hemoglobin. Further research is needed to explore the role of B cells and TLR activity in chronic inflammatory processes and in patients with chronic inflammatory diseases such as T2D.

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Lecron, Jean-Claude. "Caractérisation biologique et physico-chimique d'un facteur "prothymocyte differentiating activity" (ptda) capable de promouvoir la différenciation et l'activation de lymphocytes T humains." Poitiers, 1988. http://www.theses.fr/1988POIT2270.

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La differenciation lymphocytaire t obeit a des mecanismes complexes faisant extervenir des interactions cellulaires de contact et des facteurs solubles. Les techniques de clonage lymphocytaire t en milieu semi solide ont permis de mettre en evidence un facteur doue d'une activite differenciatrice vis a vis de prothymoxytes medullaires humains (ptda). Ce facteur est produit, par les cellules b + nulles du sang peripherique stimulees par la phytohemagglutinine. Des etudes sequentielles suggerent que la ptda agit non comme un facteur de proliferation mais comme un signal de differenciation des prothymocytes et de preactivation des lymphocytes t cd4+

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Gannon, Gregory Allan. "Peripheral blood lymphocyte trafficking and natural killer cell cytolytic activity during prolonged, exhaustive aerobic exercise, a focus on cell adhesion molecules and ß-endorphin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0002/NQ35159.pdf.

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Santoro, Lyse. "Appretement et présentation d'un anticorps monoclonal murin par une lignée monocytaire ou lymphocytaire B humaine : influence de la liaison covalente entre anticorps et fragment C3b du complément." Grenoble 1, 1994. http://www.theses.fr/1994GRE10126.

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La proteine c3 du complement influence l'elaboration de la reponse immune specifique dirigee contre un antigene defini. L'etude presentee dans cette these contribue a demontrer que le fragment c3b du complement, en se fixant de facon covalente a un antigene d'origine exogene, module l'appretement de l'antigene par une cellule presentatrice de l'antigene. Des donnees bibliographiques recentes concernant l'appretement d'antigenes, le fragment c3b et son implication dans la reponse immune specifique sont presentees dans un chapitre d'introduction. L'etude experimentale decrite a ete realisee en utilisant des anticorps monoclonaux murins comme antigenes et des cellules monocytaires ou lymphocytaires b humaines comme cellules presentatrices ; des complexes covalents anticorps monoclonaux-c3b ont ete produits et caracterises. Les resultats obtenus sont exposes dans trois chapitres. Dans un premier chapitre, des experiences montrent que la presentation d'anticorps monoclonaux murins a des cellules t humaines specifiques de ces anticorps est modulee lorsqu'ils sont complexes au fragment c3b. Puis certaines des principales etapes de l'appretement des anticorps utilises sont caracterisees dans des cellules monocytaires u937 ou lymphocytaires b humaines non specifiques de l'antigene (fixation a des recepteurs membranaires, internalisation, transit intracellulaire, modifications biochimiques) ; enfin, l'influence de la liaison covalente entre anticorps et c3b sur ces differentes etapes est mise en evidence. Des hypotheses sont proposees concernant un role chaperon de c3b

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Книги з теми "Lymphocyte activity"

Young, Neil T. Human leucocyte matching and the development of helper and cytotoxic activity by alloreactive lymphocytes. Oxford: Oxford Brookes University, 1997.

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Gillis, L. Jane. Expression and recombinase activity of RAG 1 and two splice variants of RAG 2 in mature human primary tonsilar B lymphocytes. Ottawa: National Library of Canada, 1999.

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DeKrey, Gregory K. Investigation of the mechanism of 3,3',4,4',5,5'-hexachlorobiphenyl-induced suppression of cytotoxic T lymphocyte activity in C57B1/6 mice: Endocrine and cytokine dysregulation. 1994.

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Gannon, Gregory Allan. Peripheral blood lymphocyte trafficking and natural killer cell cytolytic activity during prolonged, exhaustive aerobic exercise: A focus on cell adhesion molecules and [beta]-endorphin. 1998.

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Rider, Lisa G., and Frederick W. Miller. Outcome assessment in the idiopathic inflammatory myopathies. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0016.

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Due to their rarity, heterogeneity, and multispecialty nature, the myositis syndromes have limited data-driven consensus on appropriate outcome measures. Recently, two international, multispecialty consortia developed new tools and consensus on core set measures of myositis disease activity and damage, as well as response criteria that are now recommended for use as clinical trial endpoints but will also be useful in clinical practice. Magnetic resonance imaging, muscle ultrasound, selected laboratory tests, and immunological biomarkers—including cytokines, chemokines, lymphocyte flow cytometry, and endothelial activation markers—can all be helpful adjuncts to serum muscle enzyme levels in assessing disease activity and damage, but these have not yet been fully validated. Definitions of clinically inactive disease, complete clinical response, and remission have also been proposed but require further validation. These advances should enhance the development of therapies by standardizing our ability to demonstrate their efficacy in treating the idiopathic inflammatory myopathies.

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Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.

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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.

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Grom, Alexei A., and Athimalaipet V. Ramanan. Macrophage activation syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0168.

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Macrophage activation syndrome (MAS) is a life-threatening condition caused by excessive activation and proliferation of T lymphocytes and haemophagocytic macrophages. Although MAS has been reported in association with almost any rheumatic disease, it is by far most common in systemic juvenile idiopathic arthritis. Flares of the underlying disease or infection are most common triggers of MAS. The pathognomonic feature of MAS is typically found in bone marrow: numerous, well-differentiated macrophagic histiocytes phagocytosing normal haematopoietic elements. The expansion of these histiocytes leads to a massive systemic inflammatory reaction associated with three cardinal clinical features: severe cytopenias, liver dysfunction, and coagulopathy consistent with disseminated intravascular coagulation. Clinically, MAS is strikingly similar to the autosomal recessive disorders collectively known as familial haemophagocytic lymphohistiocytosis (FHLH). FHLH has been associated with various genetic defects affecting the cytolytic pathway. Cytolytic function is profoundly depressed in MAS patients as well, and this abnormality is caused by both genetic and acquired factors. Studies in animals suggest that uncontrolled expansion of activated CD8+ T lymphocytes secreting cytokines that activate macrophages is central to the pathophysiology of haemophagocytic syndromes. Consistent with this view, the combination of steroids and ciclosporin, an immunosuppressant that preferentially inhibits T lymphocytes, is an effective treatment for the majority of MAS patients. Patients in whom MAS remains active despite this treatment present a serious challenge and require more aggressive immunosuppression. However, in MAS triggered by infection, the optimal level of immunosuppression is difficult to determine. As a result, reported mortality rates reach 20%.

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Частини книг з теми "Lymphocyte activity"

Koldovsky, P., and U. Koldovsky. "Tests for Determination of Lymphocyte Activity." In Lymphocytes in Immunotherapy of Cancer, 44–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74225-5_5.

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Zaffaroni, M., D. Caputo, A. Ghezzi, S. Marjorio, and C. L. Cazzullo. "Lymphocyte Subpopulations as Markers of Disease Activity in Multiple Sclerosis*." In Virology and Immunology in Multiple Sclerosis: Rationale for Therapy, 35–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73032-0_6.

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Claësson, M. H., and C. Röpke. "Antiself Suppressive (Veto) Activity of Responder Cells in Mixed Lymphocyte Cultures." In Current Topics in Microbiology and Immunology, 213–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71152-7_26.

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Eichmann, Klaus. "The Control of T Lymphocyte Activity May Involve Elements of Semiosis." In The Semiotics of Cellular Communication in the Immune System, 163–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73145-7_14.

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Kaplan, Joseph. "Regulation of Lymphocyte Proliferation, Differentiation, and Functional Activity by Peptide Growth Factors." In Humoral Factors in the Regulation of Tissue Growth, 94–109. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9272-9_5.

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Ross, D. S., and T. R. Roy. "Potentiation of Rat Colon Intraepithelial Lymphocyte (IEL) Natural Killer (NK) Activity with Indomethacin." In Recent Advances in Mucosal Immunology, 527–31. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5344-7_62.

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Lahav, M., O. Epstein, N. Schoenfeld, M. Shaklai, and A. Atsmon. "Lymphocyte uroporphyrinogen synthase activity as a diagnostic test in lymphoproliferative disorders — preliminary results." In Malignant Lymphomas and Hodgkin’s Disease: Experimental and Therapeutic Advances, 171–74. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2607-6_18.

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Johnstone, Alan P. "Requirement for ADP-Ribosyltransferase Activity and Rejoining of DNA Strand Breaks During Lymphocyte Stimulation." In Proceedings in Life Sciences, 424–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70589-2_58.

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Karayiannis, Peter, Sara O’Rourke, Jenny Waters, Richard Watts, and Howard C. Thomas. "Studies of Cytotoxic T Lymphocyte Activity in Tamarins with Acute Hepatitis A Virus Infection." In Viral Hepatitis and Liver Disease, 155–57. Tokyo: Springer Japan, 1994. http://dx.doi.org/10.1007/978-4-431-68255-4_41.

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BenEzra, David, and Genia Maftzir. "Lymphocyte Activity and the Role of Humoral Factors in Patients with Chronic Ocular Inflammation." In Documenta Ophthalmologica Proceedings Series, 283–89. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3337-8_44.

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Тези доповідей конференцій з теми "Lymphocyte activity"

Filippi, J. F., D. Arnoux, N. Tubiana, B. Boutière, F. Le Caär, J. Sampol, Lab Hématol, Pr J. Sampol, and Pr Y. Carcassonne. "PLASMINOGEN ACTIVATOR ACTIVITY OF NORMAL AND MALIGNANT MONONUCLEAR HUMAN CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643167.

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Plasminogen activators (PA) are thought to play a role in the invasive and metastatic properties of many types of cancer cells. Though, discrepancies in correlations between fibrinolytic activity and metastatic potential of malignant cells have been described.In this study, we evaluated both tissue type (tPA) and urokinase type (UK) cellular PA activities in different mononuclear cell types : normal T and B human peripheral lymphocytes, B cells from patients with chronic lymphocytic leukemia (CLL), human blood monocytes, alveolar macrophages, U 937, RAJI and JM cell 1ines.Mononuclear cells were isolated by Ficoll-hypaque gradients and monocytes by plastic adhesion. T and B cells were separated by a rosetting technique using sheep red blood cells. Cellular extracts were prepared by 0.5 % Triton X 100 buffer treatment followed by sonication and centrifugation 10 ' at 2000 g. PA assays were performed on the supernatants.UK-type PA was evaluated by a liquid-phase assay in presence of human plasminogen (Kabi) and chromogenic substrate S 2251 (Kabi).tPA was determinated using a solid-phase fibrin activity assay which involves an affinity separation step and thus allows selective detection of tPA.In both cases, results were reported in international units by reference to standard curves of UK (Choay) or tPA (Kabi).In all cell types tested, PA detected was essentially urokinase-type. Highest PA activity was found in U 937 cells (0.7 IU/5×l06 cells). In normal blood lymphocytes, mean PA activity was 0.08 IU/5×l06 cells. Examination of lymphocytes from patients with CLL revealed a marked decrease in UK activity as compared to normals (< 0.01 IU/5×106 cells in more than 50 % cases).The function of PA in normal lymphocyte physiology and the potential pathogenic role of diminished PA in CLL lymphocytes remains to be investigated.

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Garcia, Salomé, Bruno Miguel Fernandes, Sara Ganhão, Raquel Ferreira, Miguel Bernardes, Georgina Terroso, and Lúcia Costa. "AB1314 ROLE OF NEUTROPHIL TO LYMPHOCYTE RATIO, MONOCYTE TO LYMPHOCYTE RATIO, PLATELET TO LYMPHOCYTE RATIO, EOSINOPHIL TO LYMPHOCYTE AND BASOPHILE TO LYMPHOCYTE RATIO IN ASSESSING DISEASE ACTIVITY IN SPONDYLOARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.2243.

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Jung, Ju-Yang, Jiwon Kim, Chang-Hee Suh, and Hyoun-Ah Kim. "AB1320 NEUTROPHIL-TO-LYMPHOCYTE RATIO AND PLATELET-TO-LYMPHOCYTE RATIO ARE ASSOCIATED WITH DISEASE ACTIVITY IN POLYMYALGIA RHEUMATICA." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5471.

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NASCIMENTO, RENAN RODRIGUES NEVES RIBEIRO DO, DANIEL VIANA SILVA E. SILVA, RAQUEL MITIE KANNO, LUIZA SÁ E. RÊGO TUPINAMBÁ, MARIANA DAVIM FERREIRA GOMES, IGOR BELTRÃO DUARTE FERNANDES, GERMANA RIBEIRO ARAÚJO CARNEIRO DE LUCENA, BRUNA SAVIOLI LOPEZ FERNANDEZ, BRUNA SAVIOLI LOPEZ FERNANDEZ, and ALEXANDRE WAGNER SILVA DE SOUZA. "MONOCYTE TO LYMPHOCYTE RATIO AND PLATELET TO LYMPHOCYTE RATIO AS A PREDICTOR OF DISEASE ACTIVITY IN TAKAYASU’S ARTERITIS." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-515.

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Okatan, IE, M. Torgutalp, A. Ateş, E. Uslu Yurteri, ME Yayla, AB Dinçer Keleşoğlu, TM Turgay, and G. Kınıklı. "AB0554 Relationship between disease activity and neutrophil-lymphocyte ratio, platelet-lymphocyte ratio and mean platelet volume in behÇet's disease." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4807.

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Bugaeva, Irine O., M. Ledvanov, and Nina V. Bogomolova. "Change in functional activity of lymphocyte chromatin activity under the influence of low-power laser radiation." In BiOS Europe '96, edited by Giulio Jori and Tiina I. Karu. SPIE, 1996. http://dx.doi.org/10.1117/12.259999.

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Elen de Pontes, Jady, Thiago Alberto Fernandes Gomes dos Santos, and Thelma Larocca Skare. "Neutrophils-to-lymphocyte and platelet-to-lymphocyte ratio and Systemic Lupus erythematosus activity: a cross-sectional study in Brazilian patients." In SBR 2021 Congresso Brasileiro de Reumatologia. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2021.1929.

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Guzmán-Guzmán, Iris Paola, Oscar Zaragoza-García, José Eduardo Navarro-Zarza, and Isela Parra-Rojas. "AB0254 NEUTROPHIL-LYMPHOCYTE RATIO AND PLATELET-LYMPHOCYTE RATIO IN PATIENTSRECEIVING ANTIRHEUMATIC THERAPY: RELATIONSHIP TO CLINICAL AND LABORATORY MARKERS OF DISEASE ACTIVITY." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7762.

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Aydar, S., S. Alataş, L. Numanoğlu, and A. Sönmezdağ. "EFFECT OF ORAL ANTICOAGULANTS ON STABLE ROSETTE FORMATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643271.

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Human peripheral blood T lymphacytes when cultered in the presence of mitogen Phytohemogglutinin (PHA) acquire the capacity to form E rosettes with sheep erythrocytes that are resistant to incubation at 37° C. Whereas human thymus lymphocytes form 37° C stable E rosettes. On the other hand, it is shown that the use of anticoagulants can prevent cancer metastases which brings forth the importance of explaining the relationship between the lymphocyte functions and anticoagulant action mecha-nismus. In order to investigate this relationship, we did a group af experiments with lymphocytes of normal children and of children with severe burn wounds. Peripheral blood lymphocytes were seperated by “Lymphoprep” centrifugation technique. The lymphocytes of normal children and patients with burn were divided in two groups: A-Activated lymphocytes: 1×106 /ml lymphocytes were cultured and activated by PHAfor 48 hours at 37° C in RPMI 1640. B-Non activated lymphocytes were in culture witout PHA. 1×10™6 M/ml warfarin sulfate was added to some of the cultures of each group prior to the culture conditions. At the end of the 48 hour incubation, heat stable rosette formation was determined by the method of Wauve and co-workers. Significantly elevated levels of heat stable rosette forming cells were found in the PHA activated culture treated with warfarin sulfate in normals and patients with burn. Although the blastic transformation of T lymphocytes was found to be depressed, heat stable rosette formation of warfarin sulfate treated lymphocytes abtained from burn patients was observed to be significantly elevated. It is concluded that warfarin sulfate increases the activity of T lymphocytes by interfering with the resynthesis of heai stable E receptors.

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Ruijtenbeek, Rob, Liesbeth Houkes-van Kerkhoff, Jeannette Oosterwijk, Liesbeth Hovestad-Bijl, Riet Hilhorst, Alejandro H. Gomez, Juan F. Rodriguez, Jesus Garcia-Donas, Bart Kiemeney, and Egbert Oosterwijk. "Abstract 5608: Correlation of phosphatase activity with lymphocyte infiltrates in metastatic renal cell carcinoma tissues." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5608.

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Звіти організацій з теми "Lymphocyte activity"

Beg, Amer A. Potentiation of T Lymphocyte Responses by Modulating NF-kB Activity in Dendritic Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada437633.

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Beg, Amer A. Potentiation of T Lymphocyte Responses by Modulating NF - Kappa Beta Activity in Dendritic Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417929.

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Mozgovaia, E. E., S. A. Bedina, A. S. Trofimenko, and I. A. Zborovskaia. Features of changes in the activity of xanthine oxidase and xanthine dehydrogenase in lymphocyte lysates and blood plasma in rheumatoid arthritis with the use of glucocorticoids. ООО ИМА-Пресс, 2018. http://dx.doi.org/10.18411/1995-4484-2018-56-3(2)-55-56.

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Banai, Menachem, and Gary Splitter. Molecular Characterization and Function of Brucella Immunodominant Proteins. United States Department of Agriculture, July 1993. http://dx.doi.org/10.32747/1993.7568100.bard.

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The BARD project was a continuation of a previous BARD funded research project. It was aimed at characterization of the 12kDa immunodominant protein and subsequently the cloning and expression of the gene in E. coli. Additional immunodominant proteins were sought among genomic B. abortus expression library clones using T-lymphocyte proliferation assay as a screening method. The 12kDa protein was identified as the L7/L12 ribosomal protein demonstrating in the first time the role a structural protein may play in the development of the host's immunity against the organism. The gene was cloned from B. abortus (USA) and B. melitensis (Israel) showing identity of the oligonucleotide sequence between the two species. Further subcloning allowed expression of the protein in E. coli. While the native protein was shown to have DTH antigenicity its recombinant analog lacked this activity. In contrast the two proteins elicited lymphocyte proliferation in experimental murine brucellosis. CD4+ cells of the Th1 subset predominantly responded to this protein demonstrating the development of protective immunity (g-IFN, and IL-2) in the host. Similar results were obtained with bovine Brucella primed lymphocytes. UvrA, GroE1 and GroEs were additional Brucella immunodominant proteins that demonstrated MHC class II antigenicity. The role cytotoxic cells are playing in the clearance of brucella cells was shown using knock out mice defective either in their CD4+ or CD8+ cells. CD4+ defective mice were able to clear brucella as fast as did normal mice. In contrast mice which were defective in their CD8+ cells could not clear the organisms effectively proving the importance of this subtype cell line in development of protective immunity. The understanding of the host's immune response and the expansion of the panel of Brucella immunodominant proteins opened new avenues in vaccine design. It is now feasible to selectively use immunodominant proteins either as subunit vaccine to fortify immunity of older animals or as diagnostic reagents for the serological survaillance.

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Bedina, S. A., E. E. Mozgovaia, A. S. Trofimenko, and I. A. Zborovskaia. The activity of enzymes of the xanthine oxidase / xanthine dehydrogenase complex in blood plasma and lymphocyte lysates in patients with seropositive and seronegative forms of rheumatoid arthritis. Академия Естествознания, 2018. http://dx.doi.org/10.18411/1996-3955-2018-6-61-64.

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Splitter, Gary, Zeev Trainin, and Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7570556.bard.

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The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.

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Malek, Thomas. Enhancing the Anti-Tumor Activity of breast Cancer-Specific Cytotoxic T Lymphocytes. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada392196.

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