Journal articles: 'Activation/tolérance des lymphocytes T'

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Bonnefoy, Nathalie, Daniel Olive, and Bernard Vanhove. "Les futures générations d’anticorps modulateurs des points de contrôle de la réponse immunitaire." médecine/sciences 35, no. 12 (December 2019): 966–74. http://dx.doi.org/10.1051/medsci/2019193.

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Les points de contrôle du système immunitaire sont des systèmes moléculaires qui complètent les processus déclenchés par la reconnaissance antigénique en contrôlant l’inhibition ou l’activation des lymphocytes et des cellules myéloïdes, notamment celle des lymphocytes T régulateurs (Treg), permettant ainsi de combiner réponses immunes et maintien de la tolérance au soi. En cancérologie, l’inhibition de points de contrôle inhibiteurs vise à amplifier les réponses immunitaires existantes dirigées contre les tumeurs. Parmi ces points de contrôle inhibiteurs, dont des antagonistes sont en utilisation clinique, se trouvent CTLA-4 (cytolytic T-lymphocyte-associated antigen 4 ou CD152), PD-1 (programmed cell death 1, ou CD279), PD-L1 (programmed cell death-ligand 1, ou CD274), LAG-3 (Lymphocyte-activation gene 3, ou CD223), TIM3 (T-cell immunoglobulin and mucin-domain containing-3), TIGIT (T cell immunoreceptor with Ig and ITIM domains), VISTA (V-domain Ig suppressor of T cell activation), ou B7/H3 (ou CD276). La stimulation de points de contrôle activateurs tels que les molécules de co-activation CD28, CD137 (aussi appelé 4-1BB), OX40 [aussi appelé tumor necrosis factor receptor superfamily, member 4 (TNFRSF4)], GITR (Glucocorticoid-induced tumor necrosis factor receptor family-related protein) ou CD40, est également testée en cancérologie, le plus souvent en combinaison avec un antagoniste de point de contrôle inhibiteur. Dans les maladies auto-immunes et inflammatoires, des antagonistes de points de contrôle activateurs (CD28, CD40) et des agonistes de points de contrôle inhibiteurs (LAG-3) sont également à l’essai. Dans cette revue, nous mettons l’accent sur certains modulateurs de points de contrôle pour lesquels le mécanisme d’action a été particulièrement étudié. Cette description ne pouvant être exhaustive, nous avons regroupé dans le Tableau I l’ensemble des anticorps monoclonaux (AcM) ou protéines recombinantes en usage clinique à notre connaissance, modulant l’action d’un point de contrôle du système immunitaire.

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Bockenstedt, Linda K., Mark A. Goldsmith, Gary A. Koretzky, and Arthur Weiss. "The Activation of T Lymphocytes." Rheumatic Disease Clinics of North America 13, no. 3 (December 1987): 411–30. http://dx.doi.org/10.1016/s0889-857x(21)00926-1.

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Bertotto, Alberto, Roberto Gerli, Luisa Lanfrancone, Silvana Crupi, Carla Arcangeli, Cristina Cernetti, Fabrizio Spinozzi, and Pietro Rambotti. "Activation of cord T lymphocytes." Cellular Immunology 127, no. 2 (May 1990): 247–59. http://dx.doi.org/10.1016/0008-8749(90)90130-j.

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Gerli, Roberto, Elisabetta Agea, Chiristopher Muscat, Rita Tognellini, Giuliana Fiorucci, Fabrizio Spinozzi, Cristina Cernetti, and Alberto Bertotto. "Activation of Cord T Lymphocytes." Cellular Immunology 148, no. 1 (April 1993): 32–47. http://dx.doi.org/10.1006/cimm.1993.1089.

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Gerli, Roberto, Elisabetta Agea, Christopher Muscat, Raffaella Ercolani, Onelia Bistoni, Rita Tognellini, Maria A. Mariggió, Fabrizio Spinozzi, and Alberto Bertotto. "Activation of Cord T Lymphocytes." Cellular Immunology 155, no. 1 (April 1994): 205–18. http://dx.doi.org/10.1006/cimm.1994.1113.

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Quintana, Ariel, D�sir�e Griesemer, Eva C. Schwarz, and Markus Hoth. "Calcium-dependent activation of T-lymphocytes." Pfl�gers Archiv - European Journal of Physiology 450, no. 1 (November 26, 2004): 1–12. http://dx.doi.org/10.1007/s00424-004-1364-4.

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Schulze, Juliane, Juliane Gellrich, Michael Kirsch, Alexander Dressel, and Antje Vogelgesang. "Central Nervous System-Infiltrating T Lymphocytes in Stroke Are Activated via Their TCR (T-Cell Receptor) but Lack CD25 Expression." Stroke 52, no. 9 (September 2021): 2939–47. http://dx.doi.org/10.1161/strokeaha.120.032763.

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Background and Purpose: T lymphocytes contribute to secondary brain damage after stroke. It has not been fully investigated whether this contribution is caused by antigen-specific or antigen-nonspecific activation of T lymphocytes. Lymphocytes from Nur77 GFP transgenic mice express a fluorescent protein upon activation via the TCR (T-cell receptor), allowing the differentiation of activation mode in a natural repertoire of immune cells and antigens. Methods: Middle cerebral artery occlusion or sham surgery was performed, and T-lymphocyte activation was analyzed by flow cytometry in the brain, spleen, and blood 16 hours, 2 days, 3 days, 4 days, and 7 days after surgery. Results: Ipsilateral hemispheric T-lymphocyte invasion peaked on day 4 poststroke. Here, we observed PD-1 (programmed cell death protein 1) expression on almost all invading T lymphocytes, while CD25 expression was low. CD25+, CD69+, or PD-1+ T lymphocytes predominantly displayed antigen-specific activation; the opposite was observed for T lymphocytes isolated from the blood. A mixed activation that favored antigen-specific activation was observed in the spleen. PD-1 was upregulated within the brain, whereas CD25 was not. Antigen-specific T lymphocytes home to the brain, while antigen-nonspecifically activated cells remain within the blood. Conclusions: Our data clearly demonstrate antigen-specific activation of T lymphocytes infiltrating ischemic brain lesions in stroke. The high expression of inhibitory PD-1 and low expression of CD25 on activated T lymphocytes in the brain most likely reflect immunosuppressive mechanisms.

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Sharom, Frances J., Anita L. H. Chiu, and T. Elaine Ross. "Gangliosides and glycophorin inhibit T-lymphocyte activation." Biochemistry and Cell Biology 68, no. 4 (April 1, 1990): 735–44. http://dx.doi.org/10.1139/o90-106.

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Increased levels of gangliosides in the serum have been linked to tumour-induced immunosuppression in vivo. Both bovine brain gangliosides and human erythrocyte glycophorin were potent inhibitors of concanavalin A, periodate, and phorbol ester – ionomycin induced activation of murine T-lymphocytes. Structurally complex gangliosides were more inhibitory, while simpler glycolipids caused less inhibition. Lymphocytes exposed to these molecules for up to 24 h could still proliferate after washing. Substantial inhibition was observed only when gangliosides and glycophorin were present during the first 18 h of activation. Studies using Quin-2 showed that gangliosides did not block the initial rapid rise in cytoplasmic Ca2+ following mitogen stimulation. Interleukin-2 (IL-2) production by ganglioside- and glycophorin-treated lymphocytes was unchanged. After treatment with gangliosides for 24 h, lymphocytes proliferated normally in response to added IL-2. These results suggest that the first round of signal transduction in response to mitogen was unaffected by gangliosides. Addition of gangliosides to activated lymphocytes in the presence of IL-2 resulted in complete inhibition of proliferation. Immunosuppression by gangliosides and glycophorin thus appears to occur at the IL-2-dependent stage of proliferation and may be partially due to IL-2 binding to these molecules. However, high levels of IL-2 failed to reverse inhibition and IL-2-dependent cell lines were much less sensitive to ganglioside inhibition than T-lymphocytes, suggesting that more than one mechanism of inhibition likely exists.Key words: gangliosides, glycophorin, T-lymphocyte, interleukin-2, interleukin-2 receptor.

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Grivel, Jean-Charles, Oxana Ivanova, Natalia Pinegina, Paul S. Blank, Alexander Shpektor, Leonid B. Margolis, and Elena Vasilieva. "Activation of T Lymphocytes in Atherosclerotic Plaques." Arteriosclerosis, Thrombosis, and Vascular Biology 31, no. 12 (December 2011): 2929–37. http://dx.doi.org/10.1161/atvbaha.111.237081.

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Pippia, Proto, Luigi Sciola, Marianne Cogoli-greuter, Maria Antonia Meloni, alessandra Spano, and Augusto Cogoli. "Activation signals of T lymphocytes in microgravity." Journal of Biotechnology 47, no. 2-3 (June 1996): 215–22. http://dx.doi.org/10.1016/0168-1656(96)01387-9.

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Arneth, Borros. "Activation of T-Lymphocytes by LDL-Cholesterol." Lipids 44, no. 4 (December 17, 2008): 311–16. http://dx.doi.org/10.1007/s11745-008-3273-3.

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Gromo, Gianni, Luca Inverardi, Robin L. Geller, Barbara J. Alter, and Fritz H. Bach. "The stepwise activation of cytotoxic T lymphocytes." Immunology Today 8, no. 9 (1987): 259–61. http://dx.doi.org/10.1016/0167-5699(87)90183-6.

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Hess, A. D., M. K. Silanskis, A. H. Esa, G. R. Pettit, and W. S. May. "Activation of human T lymphocytes by bryostatin." Journal of Immunology 141, no. 10 (November 15, 1988): 3263–69. http://dx.doi.org/10.4049/jimmunol.141.10.3263.

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Abstract The immunologic effects of bryostatin (Bryo), a PKC activator with antineoplastic activity, were assessed and compared to PMA. Bryo induced IL-2R expression on CD4+ and CD8+ human T lymphocytes with a dose response comparable to PMA. However, Bryo induced only a marginal proliferative response as compared with the vigorous response induced by PMA. Bryo mediated functional receptor expression because the proliferative response was enhanced by addition of rIL-2. Furthermore, the proliferative response was inhibited by the relatively specific Ca+, phospholipid-dependent protein kinase (PKC) inhibitor, H-7, indicating a role of PKC in Bryo-induced activation. Addition of the calcium ionophore, ionomycin, to Bryo-stimulated lymphocytes resulted in the production and secretion of IL-2 with a concomitant proliferative response. This effect of the calcium ionophore could be inhibited by cyclosporine with identical results obtained in PMA-stimulated cultures. A most intriguing finding was that Bryo could effectively antagonize PMA-induced T cell proliferation. Although this mechanism of inhibition is unclear, a discussion with respect to differential effects on potential intracellular PKC isoforms is provided. These studies indicated that Bryo has potent immunopotentiating properties that share some similar effects of the phorbol ester, PMA, but offers the additional property of modulating other phorbol ester effects on proliferation.

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Fernández, Rafael Godínez, Joaquín Azpiroz Leehan, Reyna Fierro Pastrana, and Rocío Ortíz Muñiz. "Effect of Malnutrition on K+ Current in T Lymphocytes." Clinical Diagnostic Laboratory Immunology 12, no. 7 (July 2005): 808–13. http://dx.doi.org/10.1128/cdli.12.7.808-813.2005.

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ABSTRACT Severe malnutrition in children is frequently associated with infectious diseases. Animal models have been useful for studying the effects of malnutrition. One of the immunosuppressive mechanisms of malnutrition is inhibition of the activation of T lymphocytes. The voltage-dependent K(V) potassium channels are vital for the activation of T lymphocytes. The blockade of K(V) channels inhibits the activation of T lymphocytes. Malnutrition could affect the suitable synthesis of K(V) channels in T lymphocytes, producing changes in the magnitude and/or dependency of the voltage of the K+ current. We reported a significant decrease in the K+ current and activation to a 20 mV more positive membrane potential in T lymphocytes of rats with severe malnutrition. These results indicate that the diminution in the K+ conductance by alteration of K(V) channels in severe malnutrition is one of the mechanisms that inhibit the activation of T lymphocytes.

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Brdička, Tomáš, Martin Imrich, Pavla Angelisová, Naděžda Brdičková, Ondrej Horváth, Jiří Špička, Ivan Hilgert, et al. "Non–T Cell Activation Linker (NTAL)." Journal of Experimental Medicine 196, no. 12 (December 16, 2002): 1617–26. http://dx.doi.org/10.1084/jem.20021405.

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A key molecule necessary for activation of T lymphocytes through their antigen-specific T cell receptor (TCR) is the transmembrane adaptor protein LAT (linker for activation of T cells). Upon TCR engagement, LAT becomes rapidly tyrosine phosphorylated and then serves as a scaffold organizing a multicomponent complex that is indispensable for induction of further downstream steps of the signaling cascade. Here we describe the identification and preliminary characterization of a novel transmembrane adaptor protein that is structurally and evolutionarily related to LAT and is expressed in B lymphocytes, natural killer (NK) cells, monocytes, and mast cells but not in resting T lymphocytes. This novel transmembrane adaptor protein, termed NTAL (non–T cell activation linker) is the product of a previously identified WBSCR5 gene of so far unknown function. NTAL becomes rapidly tyrosine-phosphorylated upon cross-linking of the B cell receptor (BCR) or of high-affinity Fcγ- and Fcε-receptors of myeloid cells and then associates with the cytoplasmic signaling molecules Grb2, Sos1, Gab1, and c-Cbl. NTAL expressed in the LAT-deficient T cell line J.CaM2.5 becomes tyrosine phosphorylated and rescues activation of Erk1/2 and minimal transient elevation of cytoplasmic calcium level upon TCR/CD3 cross-linking. Thus, NTAL appears to be a structural and possibly also functional homologue of LAT in non–T cells.

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Davidson, B. L., J. Faust, S. Pessano, R. P. Daniele, and G. Rovera. "Differentiation and activation phenotypes of lung T lymphocytes differ from those of circulating T lymphocytes." Journal of Clinical Investigation 76, no. 1 (July 1, 1985): 60–65. http://dx.doi.org/10.1172/jci111977.

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Pulte, Dianne, Marinus Johan Broekman, Joan Drosopoulos, Kim E. Olson, Naziba Islam, and Aaron J. Marcus. "CD39/NTPDase-1 Expression Is Associated with Activation in T-Lymphocytes." Blood 108, no. 11 (November 16, 2006): 1733. http://dx.doi.org/10.1182/blood.v108.11.1733.1733.

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Abstract CD39/NTPDase-1 is an ecto-ATP/ADPase expressed on leukocytes and endothelial cells. CD39 is the main control system for blood fluidity. CD39 on lymphocytes was first reported in 1991 by Kansas et al. However, studies of CD39 expression and activity on leukocytes have not been done. We characterized levels of CD39 expression and enzymatic activity on neutrophils (PMN), lymphocytes and lymphocyte subsets. Since inflammatory responses occur in arterial vascular disease, we also examined expression of CD39 on naive versus activated and memory lymphocytes. Lymphocytes were isolated by a histopaque procedure, and PMN by dextran gradient. B-lymphocytes were isolated using the RosetteSep B-cell kit. All cell types were confirmed to have purities of >90%. CD39 activity was assayed via our radio-thin-layer chromatographic system. CD39 expression was measured on leukocytes via FACS. PMN, monocytes, and lymphocytes were identified by their forward and side-scatter characteristics. Subsets of lymphocytes were examined via double staining for CD39 and antibodies against specific sub-types. CD39 localized to the surface of greater than 95% of neutrophils, monocytes, and B-lymphocytes. It was also present on a minority (~8%) of T-lymphocytes with no difference in frequency of expression between CD4+ and CD8+ cells. Geometric mean (GM) expression of CD39 per cell was greatest in B-lymphocytes and monocytes, lower in CD4+ cells, and lowest in CD8+ cells and PMN. Interestingly, incubation of T- lymphocytes with PHA up-regulated CD39 in CD8+ cells both in terms of number of cells expressing and GM, with expression rising to 65%. The GM increased 4-fold after 6d of stimulation with PHA. A similar but less dramatic increase was seen with LPS. This is the first time we have accomplished up-regulation of CD39 expression and enzymatic activity. Radio-TLC measurement of nucleotidase activity showed B-lymphocytes>PMN>T-lymphocytes. B-lymphocyte ADPase and ATPase activities (in pmol/min/50K cells) were 75 and 43, respectively. PMN displayed 39 (ADPase) and 22 (ATPase), while T-lymphocytes had enzymatic activity of 16 and 11.5, respectively. ADPase:ATPase ratios were similar for B-lymphocytes and PMN, but lower for T-lymphocytes (1.8 for B-lymphocytes and PMN, vs 1.45 for T-lymphocytes, p=0.03). Lymphocytes stimulated with PHA demonstrated an increase in enzyme activity of 10–20X baseline that peaked at 7–10d. ADPase:ATPase ratio was unchanged. FACS measurement showed that CD39+ lymphocytes were more often activated than CD39− lymphocytes in both CD3+ (p=0.06) and CD4+ (p=0.02) subgroups. Preliminary experiments indicated that >85% of CD39+ T-lymphocytes are CD45RO+. Importantly, this suggests that CD39 is expressed primarily on activated or memory cells in the T-lymphocyte population. Thus, CD39 is expressed on a broad variety of leukocytes. T-lymphocyte expression can be induced by stimulation with mitogens. Moreover, CD39 is present primarily on CD45RO+ T-lymphocytes. We conclude that CD39 expression can be induced by activation of the immune system. The up-regulation of CD39 on activated and memory T-lymphocytes may be a compensatory mechanism for protection from thrombosis as a consequence of inflammation. It may serve as a mechanism for metabolizing extracellular ATP and therefore decreasing the inflammatory stimulus. Abnormalities in CD39 may result in decreased nucleotidase activity and increased vulnerability to thrombosis as a consequence of inflammation.

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Cayabyab, M., J. H. Phillips, and L. L. Lanier. "CD40 preferentially costimulates activation of CD4+ T lymphocytes." Journal of Immunology 152, no. 4 (February 15, 1994): 1523–31. http://dx.doi.org/10.4049/jimmunol.152.4.1523.

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Abstract CD40 is a membrane differentiation antigen constitutively expressed on B cells that induces B cell growth and Ig synthesis after ligation with anti-CD40 mAb or with the recently identified CD40 ligand (CD40L). CD40L is rapidly induced on T cells after activation with anti-CD3 mAb or mitogens. While CD40-CD40L interactions are clearly beneficial to B cells, we speculated that a reciprocal costimulation of T cells might also occur. We have used genetic transfection to demonstrate that interactions between human small, resting T cells and CD40+ murine transfectants substantially augmented anti-CD3 induced T cell proliferation and resulted in the generation of CTL. T cell proliferation costimulated by CD40 was IL-2 dependent. The ability of CD40+ transfectants to costimulate T cell proliferation was specific in that VCAM-1+, CD54+, CD72+, CD56+, CD31+, and fas+ transfectants in the same host cells were inactive. CD4+ T cells preferentially responded to CD40 costimulation, whereas CD8+ T cells were substantially less reactive. By contrast, costimulation with B7 transfectants induced equivalent proliferation in the CD4+ and CD8+ T cell subsets. In addition, adult naive and memory T cells, as well as cord blood T cells, were responsive to CD40. These findings suggest that the CD40-CD40L costimulation pathway may allow for selective expansion of CD4+ T cells after interaction with CD40-bearing APC. The relatively restricted expression of CD40 on APC, as well as on medullary and cortical thymic epithelium, indicates a possible role for this interaction in T cell differentiation and activation.

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Atherfold, P. A., M. S. Norris, P. J. Robinson, E. W. Gelfand, and R. A. Franklin. "Calcium-induced ERK activation in human T lymphocytes." Molecular Immunology 36, no. 8 (June 1999): 543–49. http://dx.doi.org/10.1016/s0161-5890(99)00076-0.

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Plum, J., P. Van Cauwenberge, and Magda De Smedt. "Analysis of Activation Markers on Tonsillar T Lymphocytes." Acta Oto-Laryngologica 105, sup454 (January 1988): 113–17. http://dx.doi.org/10.3109/00016488809125013.

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KEMP, M., T. G. THEANDER, E. HANDMAN, A. S. HEY, J. A. L. KURTZHALS, L. HVIID, A. L. SØRENSEN, J. O. B. WERE, D. K. KOECH, and A. KHARAZMI. "Activation of Human T Lymphocytes by Leishmania Lipophosphoglycan." Scandinavian Journal of Immunology 33, no. 2 (February 1991): 219–24. http://dx.doi.org/10.1111/j.1365-3083.1991.tb03752.x.

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Kellermann, Sirid-Aimee, Cheryl L. Dell, Stephen W. Hunt, and Yoji Shimizu. "Genetic analysis of integrin activation in T lymphocytes." Immunological Reviews 186, no. 1 (August 2002): 172–88. http://dx.doi.org/10.1034/j.1600-065x.2002.18615.x.

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Cruikshank, W. W., J. S. Berman, A. C. Theodore, J. Bernardo, and D. M. Center. "Lymphokine activation of T4+ T lymphocytes and monocytes." Journal of Immunology 138, no. 11 (June 1, 1987): 3817–23. http://dx.doi.org/10.4049/jimmunol.138.11.3817.

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Abstract The function of the T4 antigen, a marker for a differentiated T cell subset, is not well understood. Our previous observation that a chemoattractant human lymphokine, lymphocyte chemoattractant factor (LCF), which selectively induces motile responses in unactivated T4+ lymphocytes, led us to investigate whether LCF could also induce T4+ cell activation. Because LCF acts selectively on T4+ cells, we next determined whether the T4 antigen has a function in this LCF-induced cellular activation. A T4+ lymphocyte migratory response is induced by divalent anti-T4 antibody, but not by corresponding Fab fragments of the same antibody. Fab fragments of anti-T4 antibody, but not Fab fragments of anti-T3 antibody, block the migratory effect of both LCF and divalent anti-T4. Furthermore, LCF but not divalent anti-T4, evokes the expression of interleukin 2 (IL 2) receptors and HLA-DR antigen on T4+ lymphocytes in 24 hr. These effects are quantitatively similar to those observed by anti-T3 antibody activation. LCF-induced IL 2 receptor expression is blocked by co-incubation with anti-T4 antibody and anti-T4 Fab fragments, whereas anti-T3 activation is not inhibitable by anti-T4 Fab fragments. Because cultured monocytes express the T4 antigen, we investigated the action of LCF on cultured monocyte migration and HLA-DR expression. Induction of monocyte migration by LCF and anti-T4 antibody increases proportionally as T4 antigen expression increases in vitro. This enhanced migration is inhibitable by anti-T4 Fab fragments. Monocyte activation, as measured by augmented HLA-DR expression 24 hr after incubation with LCF, but not anti-T4 antibody, is quantitatively similar to the effects of interferon-gamma. Augmented HLA-DR expression is blocked by anti-T4 Fab fragments but not by antibody to interferon-gamma. These studies indicate that LCF interacts with T4+ lymphocytes and monocytes to induce migration and cellular activation.

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Fleischer, B. "A novel pathway of human T cell activation via a 103 kD T cell activation antigen." Journal of Immunology 138, no. 5 (March 1, 1987): 1346–50. http://dx.doi.org/10.4049/jimmunol.138.5.1346.

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Abstract A novel triggering signal for human proliferating and cytotoxic T lymphocytes defined by a 103 kD T cell-specific activation antigen (Tp103) is described. Tp103 is expressed on all proliferating normal T cells but is not present, or present only in low amounts, on resting peripheral blood T lymphocytes. Cross-linking of T cell and Fc receptor-positive accessory or target cells by an antibody against Tp103 leads to activation of the T cell. The proliferative response is due to an autocrine IL 2-dependent mechanism and can be inhibited by antibodies against the IL 2 receptor or by Cyclosporin A. Resting Tp103-positive T cells also respond to anti-Tp103. Although Tp103 is not linked to the antigen receptor/T3 complex, triggering via Tp103 can be inhibited by modulation of the T3 molecule. Thus, Tp103 defines a new antigen-independent pathway of T cell activation that can be regulated via other T cell surface structures.

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Krinzman, S. J., G. T. De Sanctis, M. Cernadas, L. Kobzik, J. A. Listman, D. C. Christiani, D. L. Perkins, and P. W. Finn. "T cell activation in a murine model of asthma." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 3 (September 1, 1996): L476—L483. http://dx.doi.org/10.1152/ajplung.1996.271.3.l476.

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To determine the mechanisms by which inhaled antigens produce pulmonary inflammation and bronchial hyperreactivity, we have developed a murine model of asthma. BALB/c mice are sensitized and challenged with ovalbumin (OVA). Compared with mice treated with phosphate-buffered saline (PBS), OVA-treated mice developed increased lung resistance, decreased dynamic compliance, and greater methacholine reactivity. Bronchoalveolar lavage fluid revealed significant increases in the proportion of neutrophils and eosinophils. Tissue sections of OVA-treated mice demonstrated goblet cell metaplasia and focal perivascular and peribronchial infiltrates composed of lymphocytes, neutrophils, and eosinophils. Analysis of thoracic lymphocytes via flow cytometry revealed an expansion of both CD4+ and B cell populations, with increased expression of interleukin-2 receptor on CD4+ T cells, indicated increased activation. There was also increased expression of CD44 on CD4+ and CD8+ lymphocytes, suggesting an expansion of the local memory cell population. These findings support the hypothesis that activation of T lymphocytes mediates allergic pulmonary inflammation and bronchial reactivity in asthma.

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Zhang, Jimin, Satish Devadas, and Yufang Shi. "Differential roles of CD95L and TRAIL in activation-induced cell death of cytotoxic T lymphocytes (110.22)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 110.22. http://dx.doi.org/10.4049/jimmunol.188.supp.110.22.

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Abstract Cytotoxic T lymphocytes can be differentiated into type 1 (Tc1) and type 2 (Tc2) subsets as their T helper counterparts. Interestingly, our investigation in activation-induced cell death mechanisms reveals that CD95L mediates cell death in Tc1 lymphocytes and that Tc2 lymphocytes require TRAIL. Cell death in both subsets is also dependent on caspases. Inhibiting CD95L binding to its receptors in Tc1 lymphocytes from wild type mice displays altered Tc1 lymphocyte death, while Inhibiting TRAIL binding to its receptors in Tc2 lymphocytes shows altered Tc2 lymphocyte death. Activation-induced cell death in both Tc1 and Tc2 lymphocyte subsets can be blocked by pan caspase inhibitors. Moreover, Tc2 lymphocytes differentiated from TRAIL knockout mice show alleviated cell death. Rescued Tc2 lymphocytes secrete significantly higher amounts of IL-4, IL-5 and IL-10 while Tc1 lymphocytes produce higher IFN-γ and TNF-α. Our results indicate that CD95L and TRAIL play differential seminal roles in activation-induced cell death of these two cytotoxic T lymphocyte subsets, and that their different sensitivity to activation-induced cell death can alter CD8+ phenotype. With our study we conclude that Tc1 lymphocyte activation-induced cell death is mediated by CD95L while Tc2 lymphocytes undergo TRAIL-dependent activation-induced cell death.

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Leal, Vinícius Nunes Cordeiro, Edione Cristina Reis, Fernanda Pereira Fernandes, and Alessandra Pontillo. "NLRP3 inflammasome activation profile in CD4+ T and CD19+ B lymphocytes from HIV-infected patients." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 225.8. http://dx.doi.org/10.4049/jimmunol.204.supp.225.8.

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Abstract Background HIV-1 triggers inflammasome activation in myeloid cells, through NLRP3, which contributes to the first line defense against infection. However, it was postulated that NLRP3 activation could be involved in chronic inflammation and immune exhaustion in HIV-infected patients. But whether its activation occurs only in myeloid cells or also in lymphocytes is not yet understood. Considering that NLRP3 inflammasome was recently described in CD4+ T and CD19+ B lymphocytes, we hypothesize that NLRP3 inflammasome could be activated also in lymphoid cells during chronic HIV infection. Aim To evaluate NLRP3 activation in peripheral blood lymphocytes from HIV-infected patients. Methods NLRP3 inflammasome activation was evaluated in Antirretroviral-treated HIV-infected patients and healthy donors (HD) peripheral blood lymphocytes by the meaning of caspase-1 cleavage, IL-1β and IL-18 production and NLRP3+ASC+ “specks” formation. Results CD19+ B lymphocytes present a constitutive activation of NLRP3 inflammasome. But, differently from myeloid cells, LPS and β-glucan induced a higher NLRP3+ASC+ “specks” formation, caspase-1 activation and IL-1β production in B lymphocytes from HIV-infected patients compared to HD, as well as CpG induced a higher IgM production in a NLRP3-dependent way. Differently from CD19+ B lymphocytes, CD4+ T lymphocytes from HIV-infected patients present a NLRP3-independent activation of caspase-1 and IL-1β production, which was amplified by αCD3-αCD28 stimulation. Conclusions Our findings suggest that inflammasome is more activated in lymphocytes from HIV-infected patients in a cell and receptor specific manner, which could contribute to disease outcome during chronic infection.

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Diniz, Vinicius Leonardo Sousa, Anuska Marcelino Alvares-Saraiva, Tamires Duarte Afonso Serdan, Laiane Cristina dos Santos-Oliveira, Vinicius Cruzat, Tiago Bertola Lobato, Richelieau Manoel, et al. "Essential metabolism required for T and B lymphocyte functions: an update." Clinical Science 137, no. 10 (May 2023): 807–21. http://dx.doi.org/10.1042/cs20220869.

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Abstract Lymphocytes act as regulatory and effector cells in inflammation and infection situations. A metabolic switch towards glycolytic metabolism predominance occurs during T lymphocyte differentiation to inflammatory phenotypes (Th1 and Th17 cells). Maturation of T regulatory cells, however, may require activation of oxidative pathways. Metabolic transitions also occur in different maturation stages and activation of B lymphocytes. Under activation, B lymphocytes undergo cell growth and proliferation, associated with increased macromolecule synthesis. The B lymphocyte response to an antigen challenge requires an increased adenosine triphosphate (ATP) supply derived mainly through glycolytic metabolism. After stimulation, B lymphocytes increase glucose uptake, but they do not accumulate glycolytic intermediates, probably due to an increase in various metabolic pathway ‘end product’ formation. Activated B lymphocytes are associated with increased utilization of pyrimidines and purines for RNA synthesis and fatty acid oxidation. The generation of plasmablasts and plasma cells from B lymphocytes is crucial for antibody production. Antibody production and secretion require increased glucose consumption since 90% of consumed glucose is needed for antibody glycosylation. This review describes critical aspects of lymphocyte metabolism and functional interplay during activation. We discuss the primary fuels for the metabolism of lymphocytes and the particularities of T and B cell metabolism, including the differentiation of lymphocytes, stages of development of B cells, and the production of antibodies.

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Wang, Yuhuan, Penelope H. Dennehy, Harry L. Keyserling, Kevin Tang, Jon R. Gentsch, Roger I. Glass, and Baoming Jiang. "Rotavirus Infection Alters Peripheral T-Cell Homeostasis in Children with Acute Diarrhea." Journal of Virology 81, no. 8 (January 31, 2007): 3904–12. http://dx.doi.org/10.1128/jvi.01887-06.

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ABSTRACT The patterns of gene expression and the phenotypes of lymphocytes in peripheral blood mononuclear cells (PBMC) from children with diarrhea caused by rotavirus and healthy children were compared by using DNA microarray, quantitative PCR, and flow cytometry. We observed increased expression of a number of genes encoding proinflammatory cytokines and interferon or interferon-stimulated proteins and demonstrated activation of some genes involved in the differentiation, maturation, activation, and survival of B lymphocytes in PBMC of patients with rotavirus infection. In contrast, we observed a consistent pattern of lower mRNA levels for an array of genes involved in the various stages of T-cell development and demonstrated a reduction in total lymphocyte populations and in the proportions of CD4 and CD8 T lymphocytes from PBMC of patients. This decreased frequency of T lymphocytes was transient, since the proportions of T lymphocytes recovered to almost normal levels in convalescent-phase PBMC from most patients. Finally, rotavirus infection induced the activation and expression of the early activation markers CD83 and CD69 on a fraction of CD19 B cells and the remaining CD4 and CD8 T lymphocytes in acute-phase PBMC of patients; the expression of CD83 continued to be elevated and was predominantly exhibited on CD4 T lymphocytes in convalescent-phase PBMC. On the basis of these findings at the molecular, phenotypic, and physiologic levels in acute-phase PBMC, we conclude that rotavirus infection induces robust proinflammatory and antiviral responses and B-cell activation but alters peripheral T-cell homeostasis in children.

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Raju, Bindu, Chung F. Tung, Debbie Cheng, Nora Yousefzadeh, Rany Condos, William N. Rom, and Doris B. Tse. "In Situ Activation of Helper T Cells in the Lung." Infection and Immunity 69, no. 8 (August 1, 2001): 4790–98. http://dx.doi.org/10.1128/iai.69.8.4790-4798.2001.

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ABSTRACT To better understand the lung and systemic responses of helper T cells mediating memory immunity to Mycobacterium tuberculosis, we used three- and four-color flow cytometry to study the surface phenotype of CD4+ lymphocytes. Bronchoalveolar lavage (BAL) fluid and peripheral blood (PB) samples were obtained from a total of 25 subjects, including 10 tuberculosis (TB)-infected subjects, 8 purified-protein-derivative-negative subjects, and 7 purified-protein-derivative-positive subjects. In marked contrast to CD4+ lymphocytes from PB (9% ± 5% expressing CD45RA and CD29), the majority (55% ± 16%) of CD4+ lymphocytes in BAL (ALs) simultaneously expressed CD45RA, a naı̈ve T-cell marker, and CD29, members of the very late activation family. Further evaluation revealed that CD4+ ALs expressed both CD45RA and CD45RO, a memory T-cell marker. In addition, the proportion of CD4+ lymphocytes expressing CD69, an early activation marker, was drastically increased in BAL fluid (83% ± 9%) compared to PB (1% ± 1%), whereas no significant difference was seen in the expression of CD25, the low-affinity interleukin 2 receptor (34% ± 15% versus 40% ± 16%). More importantly, we identified a minor population of CD69bright CD25bright CD4+lymphocytes in BAL (10% ± 6%) that were consistently absent from PB (1% ± 1%). Thus, CD4+ lymphocytes in the lung paradoxically coexpress surface molecules characteristic of naı̈ve and memory helper T cells as well as surface molecules commonly associated with early and late stages of activation. No difference was observed for ALs obtained from TB-infected and uninfected lung segments in this regard. It remains to be determined if these surface molecules are induced by the alveolar environment or if CD4+ lymphocytes coexpressing this unusual combination of surface molecules are selectively recruited from the circulation. Our data suggest that ex vivo experiments on helper T-cell subsets that display distinctive phenotypes may be pivotal to studies on the human immune response to potential TB vaccines.

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Ronchetti, Simona, Giuseppe Nocentini, Carlo Riccardi, and Pier Paolo Pandolfi. "Role of GITR in activation response of T lymphocytes." Blood 100, no. 1 (July 1, 2002): 350–52. http://dx.doi.org/10.1182/blood-2001-12-0276.

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Abstract In this study, we describe the generation and characterization of mice in which GITR gene (TNFRSF18 [tumor necrosis factor receptor superfamily 18]), a member of the TNFRSF expressed mainly on T lymphocytes, has been ablated (GITR−/− mice). Results indicate that GITR inactivation does not impair the normal development of the lymphoid organs but modulates T-cell activation. In fact, whenGITR−/− T lymphocytes are activated by treatment with an anti-CD3 monoclonal antibody they proliferate more than wild-type cells. Moreover, activatedGITR−/− T lymphocytes express higher levels of interleukin-2 receptor, produce larger amounts of interleukin-2, and are more sensitive to activation-induced cell death than controls. These results suggest that GITR is involved in the regulation of T-cell receptor/CD3–driven T-cell activation and programmed cell death.

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Brest, Patrick, Baharia Mograbi, Véronique Hofman, Agnès Loubat, Bernard Rossi, Patrick Auberger, and Paul Hofman. "Rho GTPase Is Activated by Cytotoxic Necrotizing Factor 1 in Peripheral Blood T Lymphocytes: Potential Cytotoxicity for Intestinal Epithelial Cells." Infection and Immunity 71, no. 3 (March 2003): 1161–69. http://dx.doi.org/10.1128/iai.71.3.1161-1169.2003.

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ABSTRACT Some strains of Escherichia coli related to acute cystitis or colitis produce a toxin named cytotoxic necrotizing factor 1 (CNF-1). CNF-1 mediates its effects on epithelial cells or phagocytes via the permanent activation of small GTP-binding proteins, caused by the toxin-induced deamidation of Glu63 of p21 Rho. The behavior of peripheral blood T lymphocytes during the acute phase of bacterial colitis has been poorly investigated. Our study was conducted to test whether (i) peripheral blood T lymphocytes can be activated by CNF-1 and (ii) CNF-1-activated T lymphocytes are cytotoxic against intestinal epithelial cells. Activation of T lymphocytes by CNF-1 was assessed by electrophoresis, flow cytometry, confocal microscopy, and electron microscopy studies. Assays for migration and adherence of CNF-1-treated T lymphocytes were performed in Transwell chambers with T84 intestinal epithelial cells grown on polycarbonate semipermeable filters. CNF-1 induced a decrease in the electrophoretic mobility of the GTP-binding protein Rho in treated T lymphocytes. CNF-1 provoked an increase in the content of actin stress fibers and pseudopodia in T lymphocytes. Several adherence molecules were clustered into cytoplasmic projections in CNF-1-treated T lymphocytes and adherence of such lymphocytes on the basolateral pole of T84 was increased, resulting in cytotoxicity toward epithelial cells. Such enhanced adherence in response to CNF-1 was dependent on p42-44MAP kinase activation of T lymphocytes. Taken together, these results suggest that CNF-1, by acting on T lymphocytes, may increase in an important fashion the virulence of certain strains of E. coli against the intestinal epithelia.

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Schaller, J., Haustein UF, and H. Fiebig. "T-helper cell activation in bullous pemphigoid." Acta Dermato-Venereologica 67, no. 6 (November 1, 1987): 520–23. http://dx.doi.org/10.2340/0001555567520523.

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In 10 untreated patients suffering from acute bullous pemphigoid the number of peripheral blood T cells (CD 3), T suppressor (CD 8) and T helper cells (CD 4) as well as activation antigens (DR and Tac) bearing lymphocytes was evaluated by monoclonal antibodies. While the pan-T cell population (CD 3) and T suppressor subpopulation (CD 8) were normal, the T helper subpopulation (CD 4) and the number of DR and Tac positive lymphocytes were significantly increased in the acute stage of bullous pemphigoid when compared to the age- and sex-matched controls. Phenotypically those DR positive cells belonged to the pan-T cell population (CD 3) at 66% and to the T helper subpopulation (CD 4) at 53% respectively. Under treatment with immunosuppressants the cell counts returned to normal suggesting a T helper cell activation to be involved in the acute stage of bullous pemphigoid.

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González-Amaro, Roberto, Diana Portales-Pérez, Lourdes Baranda, Juan M. Redondo, Sara Martínez-Martínez, María Yáñez-Mó, Rosario García-Vicuña, Carlos Cabañas, and Francisco Sánchez-Madrid. "Pentoxifylline Inhibits Adhesion and Activation of Human T Lymphocytes." Journal of Immunology 161, no. 1 (July 1, 1998): 65–72. http://dx.doi.org/10.4049/jimmunol.161.1.65.

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Abstract We have herein studied the effect of pentoxifylline (PTX) on the adhesion and activation of human T lymphocytes. We found that PTX inhibited the adhesion of T cells to the β1 and β2 integrin ligands VCAM-1 and ICAM-1; this inhibitory activity was dose dependent, with a maximal effect from 12 to 24 h. We also found that PTX was able to interfere with the activation of β1 integrins induced by intracellular signals; however, the conformational change of β1 integrins induced by extracellular stimuli (e.g., activating mAbs, or Mn2+) was not significantly affected by this drug. In addition, the homotypic aggregation of T cells induced by anti-β1 and -β2 integrin chain mAbs was also inhibited by PTX. PTX had a significant inhibitory effect on the T lymphocyte expression of the activation Ags CD25 (IL-2Rα-chain), CD69 (activation-inducer molecule), and CD98 (4F2) induced by PHA. Accordingly, PTX also interfered with early cell activation events such as the rise in intracellular Ca2+ and the activation of the Na+/H+ antiporter induced by PHA and phorbol esters, respectively. Furthermore, this drug inhibited both the cell cycle progression and cell proliferation of T cells induced through the CD3/TCR complex. However, this drug did not show any effect on the cell activation/proliferation induced by PMA plus ionomycin. Our results indicate that PTX interferes efficiently with the activation and cell adhesion of human T lymphocytes. These effects may be of relevance for the clinical uses of this drug.

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Buck, J., F. Grün, F. Derguini, Y. Chen, S. Kimura, N. Noy, and U. Hämmerling. "Anhydroretinol: a naturally occurring inhibitor of lymphocyte physiology." Journal of Experimental Medicine 178, no. 2 (August 1, 1993): 675–80. http://dx.doi.org/10.1084/jem.178.2.675.

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Vitamin A (retinol) is an essential cofactor for growth of B lymphocytes in culture and for activation of T lymphocytes by antigen receptor-mediated signals. 14-hydroxy-4,14-retro-retinol (14-HRR) a metabolite of retinol, has been implicated as the intracellular mediator of this effect. Anhydroretinol (AR) is a retinol derivative with retro structure produced in activated human B lymphocytes and the insect cell lines SF 21 and Schneider S2. AR reversibly inhibits retinol- and 14-HRR-dependent effects and blocks B lymphocyte proliferation as well as activation of resting T lymphocytes. The intracellular signaling pathway blocked by AR in T cell activation is distinct from the calcineurin/interleukin 2 pathway inhibitable by cyclosporine A or FK-506.

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Inaba, K., J. W. Young, and R. M. Steinman. "Direct activation of CD8+ cytotoxic T lymphocytes by dendritic cells." Journal of Experimental Medicine 166, no. 1 (July 1, 1987): 182–94. http://dx.doi.org/10.1084/jem.166.1.182.

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Recent experiments (11-13) have shown that antigen-specific, CD8+, CD4- T lymphocytes can be induced to proliferate and become killer cells in the absence of a second population of "helper" CD8-, CD4+ cells. We have studied early events in the activation of CD4+ and CD8+ T cell subsets in the primary mixed leukocyte reaction. Dendritic cells are a major if not essential accessory cell for the activation of both subpopulations. Antigen-bearing macrophages fail to stimulate unprimed CD8+ cells, but act as targets for the sensitized cytolytic lymphocytes that are induced by dendritic cells. The initial proliferative response is comparable for CD4+ and CD8+ lymphocyte subsets. For both subpopulations, dendritic cells efficiently cluster the responding lymphocytes on the first day and induce the release of IL-2. The data indicate that CD4+ and CD8+ lymphocytes can be activated by a similar mechanism, and illustrate the special role of dendritic cells in the sensitization stage of cell-mediated immunity.

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Rubanova, Daniela, Petra Dadova, Ondrej Vasicek, and Lukas Kubala. "Pseurotin D Inhibits the Activation of Human Lymphocytes." International Journal of Molecular Sciences 22, no. 4 (February 16, 2021): 1938. http://dx.doi.org/10.3390/ijms22041938.

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Background: Pseurotins, a family of secondary metabolites of different fungi characterized by an unusual spirocyclic furanone-lactam core, are suggested to have different biological activities including the modulation of immune response. Purpose: Complex characterization of the effects of pseurotin D on human lymphocyte activation in order to understand the potential of pseurotin to modulate immune response in humans. Methods: CD4+ and CD8+ T cells and CD19+ B cells isolated from human blood were activated by various activators simultaneously with pseurotin D treatment. The effects of pseurotin were tested on the basis of changes in cell viability, apoptosis, activation of signal transducers and activators of transcription (STAT) signaling pathways, production of tumor necrosis factor (TNF)-α by T cells, expression of activation markers CD69 and CD25 on T cells and Human Leukocyte Antigen–DR isotype (HLA-DR) on B cells, and the differentiation markers CD20, CD27, CD38, and immunoglobulin (Ig) D on B cells. Results: Pseurotin D significantly inhibited the activation of both CD4+ and CD8+ human T cells complemented by the inhibition of TNF-α production without significant acute toxic effects. The Pseurotin D-mediated inhibition of T-cell activation was accompanied by the induction of the apoptosis of T cells. This corresponded with the inhibited phosphorylation of STAT3 and STAT5. In human B cells, pseurotin D did not significantly inhibit their activation; however, it affected their differentiation. Conclusions: Our results advance the current mechanistic understanding of the pseurotin-induced inhibition of lymphocytes and suggest pseurotins as new attractive chemotypes for future research in the context of immune-modulatory drugs.

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Brocker, T., and K. Karjalainen. "Signals through T cell receptor-zeta chain alone are insufficient to prime resting T lymphocytes." Journal of Experimental Medicine 181, no. 5 (May 1, 1995): 1653–59. http://dx.doi.org/10.1084/jem.181.5.1653.

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Activation studies performed with transfected T cell hybridomas and tumors revealed that chimeric molecules containing the CD3 epsilon or zeta chain intracytoplasmic portions can induce the complete effector functions normally seen only when the complete T cell receptor (TCR)/CD3 complexes of T lymphocytes are triggered. Therefore, the zeta chain, with its three antigen recognition activation motives, is thought to connect the antigen-binding Ti chains with the intracellular signaling machinery of the T cell. Here we demonstrate that the cytoplasmic portion of the TCR-zeta chain is not sufficient to activate resting T lymphocytes when cells from transgenic mice expressing a chimeric zeta receptor are used. However, after (in vivo and in vitro) activation through their endogenous TCR/CD3 complexes, the preactivated T lymphocytes could be triggered through the zeta chimera to the same extent as when they were activated through their endogenous TCR/CD3 complexes. They were able to proliferate and elicit cytotoxic functions when triggered through their zeta chimeras. These results suggest that the triggering requirements for effector functions seem to be different in resting than in activated T cells.

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Ward, S. G., and D. A. Cantrell. "Heterogeneity of the regulation of phospholipase C by phorbol esters in T lymphocytes." Journal of Immunology 144, no. 9 (May 1, 1990): 3523–28. http://dx.doi.org/10.4049/jimmunol.144.9.3523.

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Abstract In many cells, protein kinase C (PKC) activation inhibits cellular phospholipase C thereby preventing receptor-mediated phosphatidylinositol (PI) metabolism. In T lymphocytes, the T cell antigen receptor (Ti)/CD3 complex regulates PI hydrolysis and we have examined the consequences of PKC activation on Ti/CD3-mediated PI metabolism in human peripheral blood-derived T lymphocytes (T lymphoblasts) and the leukemic T cell line Jurkat. In Jurkat cells, PI metabolism after Ti/CD3 stimulation, is inhibited by PKC activation. PKC activation also inhibits calcium-induced PI metabolism in permeabilized Jurkat cells. In marked contrast, PI metabolism after Ti/CD3 stimulation in T lymphoblasts, is not inhibited by PKC activation. Moreover, in permeabilized T lymphoblasts PI metabolism can be induced by calcium in synergy with guanine 5'-O-(3-thiotrisphosphate) via a PKC-insensitive mechanism. The different effect of PKC stimulation on PI metabolism in Jurkat cells and T lymphoblasts reveals heterogeneity of PLC regulation in T lymphocytes. The data also indicate that the role of PKC as a regulator of Ti/CD3 signal transduction can differ depending on cell type.

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Malek, T. R., E. M. Shevach, and K. M. Danis. "Activation of T lymphocytes through the Ly-6 pathway is defective in A strain mice." Journal of Immunology 143, no. 2 (July 15, 1989): 439–45. http://dx.doi.org/10.4049/jimmunol.143.2.439.

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Abstract The Ly-6 alloantigens have been shown to participate in the process of T cell activation based on the ability of anti-Ly-6 mAb to induce IL-2 production and proliferation of T lymphocytes. In the present investigation we have demonstrated that peripheral T lymphocytes from A strain mice exhibited abnormally low proliferative responses after stimulation through Ly-6A/E and Ly-6C molecules when compared to responses of T cells from numerous other mouse strains. The abnormal activation of the Ly-6 pathway of A strain T cells was not due to ineffective FcR cross-linking of the anti-Ly-6 mAb, to inappropriate cellular expression of the Ly-6A/E alloantigen in A strain T cells, or to an active suppressive phenomenon. T lymphocytes from A strain mice proliferated normally when the cells were activated by mAb to Thy-1 or the CD3/TCR complex suggesting that A strain mice did not exhibit a generalized T cell activation defect. Cell separation studies of T cells and accessory cells demonstrated that this defect was quantitative, rather than qualitative, and that it was complex, residing at both the T cell and accessory cell levels. These results suggest that activation of T lymphocytes via the Ly-6 molecule may involve a signaling pathway and/or cell-cell interactions distinct from those required for optimal activation via CD3/TCR.

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Alam, Antoine, Luchino Y. Cohen, Salah Aouad, and Rafick-Pierre Sékaly. "Early Activation of Caspases during T Lymphocyte Stimulation Results in Selective Substrate Cleavage in Nonapoptotic Cells." Journal of Experimental Medicine 190, no. 12 (December 20, 1999): 1879–90. http://dx.doi.org/10.1084/jem.190.12.1879.

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Apoptosis induced by T cell receptor (TCR) triggering in T lymphocytes involves activation of cysteine proteases of the caspase family through their proteolytic processing. Caspase-3 cleavage was also reported during T cell stimulation in the absence of apoptosis, although the physiological relevance of this response remains unclear. We show here that the caspase inhibitor benzyloxycarbonyl (Cbz)-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD) blocks proliferation, major histocompatibility complex class II expression, and blastic transformation during stimulation of peripheral blood lymphocytes. Moreover, T cell activation triggers the selective processing and activation of downstream caspases (caspase-3, -6, and -7), but not caspase-1, -2, or -4, as demonstrated even in intact cells using a cell-permeable fluorescent substrate. Caspase-3 processing occurs in different T cell subsets (CD4+, CD8+, CD45RA+, and CD45RO+), and in activated B lymphocytes. The pathway leading to caspase activation involves death receptors and caspase-8, which is also processed after TCR triggering, but not caspase-9, which remains as a proenzyme. Most importantly, caspase activity results in a selective substrate specificity, since poly(ADP-ribose) polymerase (PARP), lamin B, and Wee1 kinase, but not DNA fragmentation factor (DFF45) or replication factor C (RFC140), are processed. Caspase and substrate processing occur in nonapoptotic lymphocytes. Thus, caspase activation is an early and physiological response in viable, stimulated lymphocytes, and appears to be involved in early steps of lymphocyte activation.

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Miscia, Sebastiano, Angela Di Baldassarre, Giuseppe Sabatino, Ezio Bonvini, Rosa Alba Rana, Marco Vitale, Valentina Di Valerio, and Francesco Antonio Manzoli. "Inefficient Phospholipase C Activation and Reduced Lck Expression Characterize the Signaling Defect of Umbilical Cord T Lymphocytes." Journal of Immunology 163, no. 5 (September 1, 1999): 2416–24. http://dx.doi.org/10.4049/jimmunol.163.5.2416.

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Abstract Adult and neonatal immunocompetent cells exhibit important functional distinctions, including differences in cytokine production and susceptibility to tolerance induction. We have investigated the molecular features that characterize the immune response of cord blood-derived T lymphocytes compared with that of adult T lymphocytes. Our findings demonstrate that phospholipase C (PLC) isozymes, which play a pivotal role in the control of protein kinase C activation and Ca2+ mobilization, are differently expressed in cord and adult T lymphocytes. PLCβ1 and δ1 are expressed at higher levels in cord T cells, while PLCβ2 and γ1 expression is higher in adult T lymphocytes. PLCδ2 and γ2 appear to be equally expressed in both cell types. In addition, a functional defect in PLC activation via CD3 ligation or pervanadate treatment, stimuli that activate tyrosine kinases, was observed in cord blood T cells, whereas treatment with aluminum tetrafluoride (AlF4−), a G protein activator, demonstrated a similar degree of PLC activation in cord and adult T cells. The impaired PLC activation of cord blood-derived T cells was associated with a a very low expression of the Src kinase, Lck, along with a reduced level of ZAP70. No mitogenic response to CD3 ligation was observed in cord T cells. However, no signaling defect was apparent downstream of PLC activation, as demonstrated by the mitogenic response of cord T cells to the pharmacologic activation of protein kinase C and Ca2+ by treatment with PMA and ionomycin. Thus, neonatal cord blood-derived T cells show a signaling immaturity associated with inadequate PLCγ activation and decreased Lck expression.

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Safronova, Eleonora A., and Liana V. Ryabova. "Features of T cell immunity depending on the content of natural killer cells in patients with acute coronary syndrome following COVID-19." Russian Journal of Immunology 26, no. 3 (August 11, 2023): 389–96. http://dx.doi.org/10.46235/1028-7221-9640-fot.

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We examined 65 men with unstable angina and acute myocardial infarction (acute coronary syndrome - ACS) from 40 to 65 years old who had previously had COVID-19 and 20 people with ACS who had not undergone COVID-19. All persons also had hypertension, and they required stenting of the coronary arteries within the next 3 days after admission to the hospital. From the immunological parameters by flow cytometry on the Navios cytofluorimeter (BeckmanCoulter, USA), according to the standardized technology for assessing the lymphocytic link of immunity [1], the following were determined: ), CD45+ CD3+ CD8+ (cytotoxic T-lymphocytes), CD45+CD3-CD19+ (B-lymphocytes), CD45+CD3+CD16+CD56+ (TNK cells), CD45+CD3-CD16+CD56+ (natural killer cells), CD45+ CD3+CD4+CD25+CD127- (T-regulatory cells), CD45+ CD3+CD4+CD25+ (T-lymphocytes - early activation), CD45+CD3+HLA-DR (T-lymphocytes - late activation). All patients were divided into groups depending on the content of NK cells (natural killer cells). Patients who have had COVID-19 have 3 phenotypes of disorders (decreased NK cell count, normal and increased), while non-survivors have 2 phenotypes (decreased NK cell count and normal). The most severe condition and severity of immune disorders were found in patients who had undergone COVID-19. In patients with acute coronary syndrome and COVID-19, predominantly with normal and elevated levels of NK cells, compared with ACS patients without COVID-19, a more severe course of the disease was observed - patients with acute myocardial infarction prevailed, they had a higher mortality rate, the duration of treatment was increased, and stent thrombosis was also more common. In persons with ACS and COVID-19 with elevated NK cells, the maximum decrease in the T-cell immunity was observed: T-lymphocytes of general, T-lymphocytes-helpers, T-cytotoxic lymphocytes, T-lymphocytes of early activation, T-regulatory cells in absolute numbers compared to other groups. The lowest immunoregulatory index and, at the same time, the maximum number of T-NK-lymphocytes were observed in persons who had undergone COVID-19 and had reduced NK cells. The minimum number of T-NK lymphocytes was recorded in patients with low NK cells who did not have COVID-19. Minimal T-lymphocytes (CD45+CD3+CD4+HLA-DR+) of late activation were found in people who recovered from COVID-19 with elevated and normal NK cells. The lowest number of late activation regulatory T cells was observed in patients who did not have COVID-19, but were vaccinated, and had a normal content of NK cells. The study also allows us to more clearly define the groups of patients with ACS who need additional immunocorrection.

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Hsueh, Y. P., and M. Z. Lai. "Overexpression of activation transcriptional factor 1 in lymphomas and in activated lymphocytes." Journal of Immunology 154, no. 11 (June 1, 1995): 5675–83. http://dx.doi.org/10.4049/jimmunol.154.11.5675.

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Abstract cAMP-regulated gene expression always involves a conserved cAMP-responsive element (CRE) present in the promoter of cAMP-inducible genes. Two of the highly related proteins, cyclic AMP-responsive element binding protein (CREB) and activation transcriptional factor 1 (ATF-1), have been shown to activate transcription in response to cAMP by interacting with CRE. However, ATF-1 is a much weaker mediator of cAMP response, and its functional role in vivo remains unclear. Here we report a significant enhancement of ATF-1 expression in most transformed lymphocytes. Little variation in CREB level was observed, however. The activation of normal T lymphocytes induced a transient increase of ATF-1 expression to a level comparable to that of T lymphomas. Activation had no effect on the ATF-1 level of transformed T lymphocytes. The induction of ATF-1 required the costimulation of normal T lymphocytes with TPA and A23187. TPA, Ca2+ ionophore, or cAMP alone did not stimulate ATF-1 expression in normal lymphocytes. Nuclear run-on assay indicates that the increased ATF-1 expression in T cell lymphomas and in activated splenic T lymphocytes was not due to an enhanced transcription. Instead, an increase in ATF-1 mRNA stability was found in these lymphocytes. The regulation of ATF-1 expression through RNA stability in cells of different states suggests that ATF-1 may play an active role in cell growth and differentiation.

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Dobrynina, M. A., A. V. Zurochka, M. V. Komelkova, Sh Luo, V. A. Zurochka, Hu Desheng, L. V. Ryabova, and A. P. Sarapultsev. "Studies of CD45+ and CD46+ expression on the peripheral blood lymphocyte subsets of the post-COVID patients." Russian Journal of Immunology 25, no. 4 (October 7, 2022): 431–36. http://dx.doi.org/10.46235/1028-7221-1160-soc.

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The SARS-CoV-2 virus can enter the cells using S1 viral spike (S) protein, not only by binding to ACE2, but also through other cellular receptors. These candidate receptors include CD46, which, like CD45, belongs to pan-leukocyte receptors and is expressed on all types of lymphocytes. In turn, SARS-CoV-2 infection is accompanied by damage to almost all compartments of the immune system, mainly T lymphocytes. The purpose of the study was to evaluate the expression levels of CD45+ and CD46+ in various subpopulations of lymphocytes in patients who had undergone SARS-CoV-2 infection. 72 patients who had undergone SARS-CoV-2 infection were examined. Using flow cytometry technique, we determined CD45+ and CD46+ (panleukocyte marker for lymphocyte gating), CD45+ and CD46+, CD3+ (T lymphocytes), CD45+ and CD46+, CD3+, CD4+ (helper inducers), CD45+ and CD46+, CD3+, CD8+ (cytotoxic T-lymphocytes), CD45+ and CD46+, CD3+, CD56+ (TNK cells) CD45+ and CD46+, CD3-, CD56+ (natural killers), CD45+ and CD46+, CD3-, CD19+ (B lymphocytes), CD45+ and CD46+, CD3+, CD4+, CD25+ (activated helpers, early activation of lymphocytes), CD45+ and CD46+, CD3+, HLA-DR (activated T lymphocytes late activation of lymphocytes). Our studies have shown that a decrease in CD46+ expression in T lymphocytes (CD3+) is accompanied by similar decrease of its expression in cytotoxic T lymphocytes (CD3+, CD8+), TNK (CD3+, CD56+), as well as in helpers T carrying markers of early activation (CD3+, CD4+, CD25+). At the same time, the most pronounced decrease was observed both among total T lymphocytes and cytotoxic T cells. In these patients, the expression level of CD46+ in B lymphocytes was slightly increased. Recent data suggest that there is no involvement of CD46 receptor on B lymphocytes. Our data suggest that the SARS-CoV-2 virus may affect the CD46 receptor. Such exposure may lead to promotion of the long-COVID (post-COVID) symptoms in such patients, thus requiring new approaches to correction of these disorders.

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Cogoli, Augusto. "The Activation of T Lymphocytes in Space - An Overview." Biological Sciences in Space 7, no. 1 (1993): 1–7. http://dx.doi.org/10.2187/bss.7.1.

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Al-Yassin, Ghassan A., and Peter A. Bretscher. "Does T Cell Activation Require a Quorum of Lymphocytes?" Journal of Immunology 201, no. 10 (November 5, 2018): 2855–61. http://dx.doi.org/10.4049/jimmunol.1800805.

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DECALLONNE, B., and C. MATHIEU. "Defective Activation-Induced Cell Death in NOD T Lymphocytes." Annals of the New York Academy of Sciences 1005, no. 1 (November 2003): 176–77. http://dx.doi.org/10.1196/annals.1288.021.

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Miller, Richurd A., Gonzalo Gorcia, Christopher J. Kirk, and Jacek M. Witkowski. "Early activation defects in T lymphocytes from aged mice." Immunological Reviews 160, no. 1 (December 1997): 79–90. http://dx.doi.org/10.1111/j.1600-065x.1997.tb01029.x.

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FERON, E. J., V. L. CALDER, and S. L. LIGHTMAN. "Oligoclonal activation of CD4+ T lymphocytes in posterior uveitis." Clinical & Experimental Immunology 99, no. 3 (June 28, 2008): 412–18. http://dx.doi.org/10.1111/j.1365-2249.1995.tb05566.x.

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Journal articles on the topic 'Activation/tolérance des lymphocytes T'

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