Regulatory B cells shape the development of Th2 immune responses in BALB/c mice infected with Leishmania major through IL-10 production.
Recent evidence indicates that B cells are required for susceptibility to infection with Leishmania major in BALB/c mice. In this study, we analyzed the role of the IL-10 produced by B cells in this process. We showed that B cells purified from the spleen of BALB/c mice produced IL-10 in response to stimulation with L. major in vitro. In vivo, early IL-10 mRNA expression is detected after L. major infection in B cells from draining lymph nodes of susceptible BALB/c, but not of resistant C57BL/6 mice. Although adoptive transfer of naive wild-type B cells prior to infection in B cell-deficient BALB/c mice restored Th2 cell development and susceptibility to infection with L. major of these otherwise resistant mice, adoptive transfer of IL-10(-/-) B cells mice did not. B cells stimulated by L. major, following in vitro or in vivo encounter, express the CD1d and CD5 molecules and the IL-10 produced by these cells downregulate IL-12 production by L. major-stimulated dendritic cells. These observations indicate that IL-10 secreting B cells are phenotypically and functionally regulatory B cells. Altogether these results demonstrate that the IL-10 produced by regulatory CD1d+ CD5+ B cells in response to L. major is critical for Th2 cell development in BALB/c mice.
Ronet
Catherine
C
World Health Organization Immunology Research and Training Center, University of Lausanne, Epalinges, Switzerland.
Hauyon-La Torre
Yazmin
Y
Revaz-Breton
Mélanie
M
Mastelic
Béatris
B
Tacchini-Cottier
Fabienne
F
Louis
Jacques
J
Launois
Pascal
P
D019264:Adoptive Transfer; D000818:Animals; D055610:Antigens, CD1d; D001402:B-Lymphocytes / Q000276:immunology* / Q000469:parasitology / Q000637:transplantation; D018956:CD5 Antigens; D004198:Disease Susceptibility / Q000276:immunology; D016753:Interleukin-10 / Q000096:biosynthesis*; D018320:Leishmania major / Q000276:immunology; D016773:Leishmaniasis, Cutaneous / Q000209:etiology / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018418:Th2 Cells / Q000166:cytology / Q000276:immunology*
D055610:Antigens, CD1d; D018956:CD5 Antigens; D016753:Interleukin-10