Regulatory B cells shape the development of Th2 immune responses in BALB/c mice infected with Leishmania major through IL-10 production.

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Serval ID
serval:BIB_760324EA3813
Type
Article: article from journal or magazin.
Collection
Publications
Title
Regulatory B cells shape the development of Th2 immune responses in BALB/c mice infected with Leishmania major through IL-10 production.
Journal
Journal of Immunology
Author(s)
Ronet C., Hauyon-La Torre Y., Revaz-Breton M., Mastelic B., Tacchini-Cottier F., Louis J., Launois P.
ISSN
1550-6606[electronic]
Publication state
Published
Issued date
2010
Peer-reviewed
Oui
Volume
184
Number
2
Pages
886-894
Language
english
Abstract
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.
Pubmed
Web of science
Open Access
Yes
Create date
02/02/2010 14:10
Last modification date
20/08/2019 14:33
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