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Blood, 1 December 2008, Vol. 112, No. 12, pp. 4555-4564. Prepublished online as a Blood First Edition Paper on September 18, 2008; DOI 10.1182/blood-2008-02-140087. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2008-02-140087v1 112/12/4555    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Tretter, T. Articles by Lorenz, H.-M. Search for Related Content PubMed PubMed Citation Articles by Tretter, T. Articles by Lorenz, H.-M. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Induction of CD4+ T-cell anergy and apoptosis by activated human B cells Theresa Tretter1, Ram K. C. Venigalla1, Volker Eckstein2, Rainer Saffrich2, Serkan Sertel3, Anthony D. Ho2, and Hanns-Martin Lorenz1 Divisions of1 Rheumatology and 2 Hematology and Oncology, Department of Medicine V, and 3 Department of Otolaryngology, Clinics of Head and Neck Surgery, University of Heidelberg, Heidelberg, Germany 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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