Induction of CD4+ T-cell anergy and apoptosis by activated human B cells Export

@article{citeulike:5287711, abstract = {B cells are well-known mediators of humoral immunity and serve as costimulators in the generation of T cell-mediated responses. In several mouse models, however, it was observed that B cells can also down-regulate immune reactions, suggesting a dual role for B cells. Due to this discrepancy and so far limited data, we directly tested the effects of primary human B cells on activated CD4+ T helper cells in vitro. We found that under optimal costimulation large, activated CD25+ B cells but not small CD25- B cells induced temporary T-cell anergy, determined by cell division arrest and down-regulation of cytokine production. In addition, large CD25+ B cells directly induced CD95-independent apoptosis in a subpopulation of activated T cells. Suppression required direct B-T-cell contact and was not transferable from T to T cell, excluding potential involvement of regulatory T cells. Moreover, inhibitory effects involved an IL-2-dependent mechanism, since decreasing concentrations of IL-2 led to a shift from inhibitory toward costimulatory effects triggered by B cells. We conclude that activated CD25+ B cells are able to costimulate or down-regulate T-cell responses, depending on activation status and environmental conditions that might also influence their pathophysiological impact. 10.1182/blood-2008-02-140087}, author = {Tretter, Theresa and Venigalla, Ram K. C. and Eckstein, Volker and Saffrich, Rainer and Sertel, Serkan and Ho, Anthony D. and Lorenz, Hanns-Martin}, citeulike-article-id = {5287711}, citeulike-linkout-0 = {http://dx.doi.org/10.1182/blood-2008-02-140087}, citeulike-linkout-1 = {http://bloodjournal.hematologylibrary.org/cgi/content/abstract/112/12/4555}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/18802006}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=18802006}, day = {1}, doi = {10.1182/blood-2008-02-140087}, journal = {Blood}, keywords = {b-cells, breg}, month = {December}, number = {12}, pages = {4555--4564}, posted-at = {2009-07-28 07:49:41}, priority = {2}, title = {Induction of CD4+ T-cell anergy and apoptosis by activated human B cells}, url = {http://dx.doi.org/10.1182/blood-2008-02-140087}, volume = {112}, year = {2008} }

TY - JOUR ID - citeulike:5287711 L3 - citeulike-article-id:5287711 N2 - B cells are well-known mediators of humoral immunity and serve as costimulators in the generation of T cell-mediated responses. In several mouse models, however, it was observed that B cells can also down-regulate immune reactions, suggesting a dual role for B cells. Due to this discrepancy and so far limited data, we directly tested the effects of primary human B cells on activated CD4+ T helper cells in vitro. We found that under optimal costimulation large, activated CD25+ B cells but not small CD25- B cells induced temporary T-cell anergy, determined by cell division arrest and down-regulation of cytokine production. In addition, large CD25+ B cells directly induced CD95-independent apoptosis in a subpopulation of activated T cells. Suppression required direct B-T-cell contact and was not transferable from T to T cell, excluding potential involvement of regulatory T cells. Moreover, inhibitory effects involved an IL-2-dependent mechanism, since decreasing concentrations of IL-2 led to a shift from inhibitory toward costimulatory effects triggered by B cells. We conclude that activated CD25+ B cells are able to costimulate or down-regulate T-cell responses, depending on activation status and environmental conditions that might also influence their pathophysiological impact. 10.1182/blood-2008-02-140087 IS - 12 JF - Blood EP - 4564 TI - Induction of CD4+ T-cell anergy and apoptosis by activated human B cells VL - 112 SP - 4555 KW - b-cells KW - breg AU - Tretter, Theresa AU - Venigalla, Ram AU - Eckstein, Volker AU - Saffrich, Rainer AU - Sertel, Serkan AU - Ho, Anthony AU - Lorenz, Hanns-Martin PY - 2008/12/01/ UR - http://dx.doi.org/10.1182/blood-2008-02-140087 ER -