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¹ The Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College of Science Technology and Medicine, London W6 8 LH, United Kingdom
² Institute of Cell Animal and Population Biology, University of Edinburgh, Ashworth Laboratories, Edinburgh EH93JT, United Kingdom

Address correspondence to C. Mauri at her present address, Centre for Rheumatology Research, The Windeyer Institute of Medical Science, 46 Cleveland Street, London W1T 4JF. Phone: 44-207-679-9670; Fax: 44-207-679-9143; E-mail: c.mauri{at}ucl.ac.uk; or M. Londei at his present address, Institute of Child Health, University College London, 30 Guilford Street, London WC1N 1EH, UK. Phone: 44-207-905-2182; Fax: 44-207-905-2316; E-mail: m.londei{at}ich.ucl.ac.uk

In this study we have shown that activation of arthritogenic splenocytes with antigen and agonistic anti-CD40 gives raise to a B cell population that produce high levels of interleukin (IL)-10 and low levels of interferon (IFN)-. Transfer of these B cells into DBA/1-TcR-ß-Tg mice, immunized with bovine collagen (CII) emulsified in complete Freund's adjuvant inhibited T helper type 1 differentiation, prevented arthritis development, and was also effective in ameliorating established disease. IL-10 is essential for the regulatory function of this subset of B cells, as the B cells population isolated from IL-10 knockout mice failed to mediate this protective function. Furthermore, B cells isolated from arthritogenic splenocytes treated in vitro with anti–IL-10/anti–IL-10R were unable to protect recipient mice from developing arthritis. Our results suggest a new role of a subset of B cells in controlling T cell differentiation and autoimmune disorders.

Key Words: autoimmunity • immunoregulation • B cells • interleukin 10 • CD40

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