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* I. Medical Department, Johannes Gutenberg-University Mainz, Obere Zahlbacher Str. 63, Mainz, Germany;
Institute for Genetics, and
Center for Molecular Medicine Cologne (CMMC) University of Cologne, Cologne, Germany;
Department of Pathology, Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland;
¶ Department of Dermatology, University of Cologne, Kerpener Str. 62, Cologne, Germany;
|| Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115;
# Faculty of Life Sciences, University of Manchester, Simon Building, Brunswick Street, Manchester, United Kingdom; and
** University of Edinburgh, Institute of Immunology and Infection Research, School of Biological Sciences, Edinburgh, United Kingdom
B cells have been shown in various animal models to induce immunological tolerance leading to reduced immune responses and protection from autoimmunity. We show that interaction of B cells with naive T cells results in T cell triggering accompanied by the expression of negative costimulatory molecules such as PD-1, CTLA-4, B and T lymphocyte attenuator, and CD5. Following interaction with B cells, T cells were not induced to proliferate, in a process that was dependent on their expression of PD-1 and CTLA-4, but not CD5. In contrast, the T cells became sensitive to Ag-induced cell death. Our results demonstrate that B cells participate in the homeostasis of the immune system by ablation of conventional self-reactive T cells.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was funded by the FP6 Marie Curie Research Training Network MRTN-CT-2004-005632, the Deutsche Forschungsgemeinschaft grant SFB548, and by funds from the Böhringer Ingelheim Stiftung (to A.W.).
2 Address correspondence and reprint requests to Dr. Ari Waisman, First Medical Department, University of Mainz, Obere Zahlbacherstr. 63, 55131 Mainz, Germany. E-mail address: waisman{at}uni-mainz.de
3 Abbreviations used in this paper: EAE, experimental autoimmune encephalomyelitis; MBP, myelin basic protein; MOG, myelin oligodendrocyte glycoprotein; AICD, Ag-induced cell death; Ii, invariant chain; sc, spinal cord; BM, bone marrow; DC, dendritic cell; WT, wild type; Treg, regulatory T cell; c-Flip, cellular FLICE-inhibitory protein; MHCII, MHC class II; BTLA, B and T lymphocyte attenuator.
4 The online version of this article contains supplemental material.
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