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B Cells Amplify IFN- Production By T Cells via a TNF--Mediated Mechanism¹

Laurence C. Menard^*, Laurie A. Minns^*, Sylvie Darche, Daniel W. Mielcarz^*, David M. Foureau^*, David Roos, Florence Dzierszinski, Lloyd H. Kasper^* and Dominique Buzoni-Gatel^2,

^* Departments of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 03756; Unité de Réponse Précoce aux Parasites et Immunopathologie, Institut Pasteur-Institut National de la Recherche Agronomique, Paris, France; Lynch Laboratories, Department of Biology, University of Pennsylvania, Philadelphia, PA 19104; and McGill University, Institute of Parasitology, Quebec, Canada

Aside from being the precursors of the Ab-secreting cells, B cells are engaged in other immune functions such as Ag presentation to T cells or cytokine production. These functions may contribute to the pathogenic role of B cells in a wide range of autoimmune diseases. We demonstrate that B cells acquire the capacity to amplify IFN- production by CD4 and CD8 T cells during the course of the Th1 inflammatory response to Toxoplasma gondii infection. Using the two following different strategies, we observed that B cells from T. gondii-infected mice, but not from naive mice, induce higher IFN- expression by splenic host T cells: 1) reconstitution of B cell-deficient mice with B cells expressing an alloantigen different from the recipients, and 2) adoptive transfer of B and T cells into RAG^–/– mice. In vitro assays allowing the physical separation of T and B cells demonstrate that Ag-primed B cells enhance IFN- production by T cells in a contact-dependent fashion. Using an OVA-transgenic strain of T. gondii and OVA-specific CD4 T cells, we observed that the proinflammatory effect of B cells is neither Ag specific nor requires MHCII expression. However, TNF- expressed on the surface of B cells appears to mediate in part the up-regulation of IFN- by the effector 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 supported by National Institutes of Health Grant AI19613.

² Address correspondence and reprint requests to Dr. Dominique Buzoni-Gatel, Unité de Réponse Précoce aux Parasites et Immunopathologie, Institut Pasteur, 28 rue du Docteur Roux, 75015 Paris, France. E-mail address: buzoni{at}pasteur.fr

³ Abbreviations used in this paper: RA, rheumatoid arthritis; MLN, mesenteric lymph node; WT, wild type.

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