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Leishmania major-Specific B Cells Are Necessary for Th2 Cell Development and Susceptibility to L. major LV39 in BALB/c Mice¹

Catherine Ronet^2,*,, Heike Voigt^2,*,, Hayo Himmelrich^*,, Marie-Agnès Doucey^3,, Yazmin Hauyon-La Torre^*,, Mélanie Revaz-Breton^*,, Fabienne Tacchini-Cottier^*,, Claude Bron, Jacques Louis and Pascal Launois^4,*,

^* World Health Organization-Immunology Research and Training Centre, and Department of Biochemistry, University of Lausanne, Epalinges, Switzerland; and Unit of "Early responses to parasites and immunopathology," Department of Parasitology and Mycology, Institut Pasteur, Paris, France

B lymphocytes are considered to play a minimal role in host defense against Leishmania major. In this study, the contribution of B cells to susceptibility to infection with different strains of L. major was investigated in BALB/c mice lacking mature B cells due to the disruption of the IgM transmembrane domain (µMT). Whereas BALB/c µMT remained susceptible to infection with L. major IR173 and IR75, they were partially resistant to infection with L. major LV39. Adoptive transfer of naive B cells into BALB/c µMT mice before infection restored susceptibility to infection with L. major LV39, demonstrating a role for B cells in susceptibility to infection with this parasite. In contrast, adoptive transfer of B cells that express an IgM/IgD specific for hen egg lysozyme (HEL), an irrelevant Ag, did not restore disease progression in BALB/c µMT mice infected with L. major LV39. This finding was likely due to the inability of HEL Tg B cells to internalize and present Leishmania Ags to specific T cells. Furthermore, specific Ig did not contribute to disease progression as assessed by transfer of immune serum in BALB/c µMT mice. These data suggest that direct Ag presentation by specific B cells and not Ig effector functions is involved in susceptibility of BALB/c mice to infection with L. major LV39.

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 Grant 310000-107719 from the Swiss National Foundation and by the Institut Pasteur.

² C.R. and H.V. contributed equally to this work.

³ Current address: Protein Analysis Facility-Centre for Integrative Genomics, Le Génopode, CH1015 Lausanne, Switzerland.

⁴ Address correspondence and reprint requests to Dr. Pascal Launois, World Health Organization-Immunology Research and Training Centre, University of Lausanne, Ch. des boveresses 155, 1066 Epalinges, Switzerland. E-mail address: p.launois{at}unil.ch

⁵ Abbreviations used in this paper: DC, dendritic cell; HEL, hen egg lysozyme; Tg, transgenic; LN, lymph node; LACK, Leishmania-activated C kinase; MFI, mean fluorescence intensity.