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A Regulatory B Cell Subset with a Unique CD1dhiCD5+ Phenotype Controls T Cell-Dependent Inflammatory Responses
Koichi Yanaba,1,3 Jean-David Bouaziz,1,3 Karen M. Haas,1 Jonathan C. Poe,1 Manabu Fujimoto,2 and Thomas F. Tedder1,*
1Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA
2Department of Dermatology, Kanazawa University Graduate School of Medical Science, Ishikawa 920-8641, Japan
3These authors contributed equally to this work.
*Correspondence: thomas.tedder@duke.edu
DOI 10.1016/j.immuni.2008.03.017
SUMMARY
B cells mediate multiple functions that influence immune and inflammatory responses. In this study, T cell-mediated inflammation was exaggerated in CD19-deficient (Cd19-/-) mice and wild-type mice depleted of CD20+ B cells, whereas inflammation was substantially reduced in mice with hyperactive B cells as a result of CD19 overexpression (hCD19Tg). These inflammatory responses were negatively regulated by a unique CD1dhiCD5+ B cell subset that was absent in Cd19/ mice, represented only 1%–2%of spleen B220+ cells in wild-type mice, but was expanded to 10% of spleen B220+ cells in hCD19Tg mice. Adoptive transfer of these CD1dhiCD5+ B cells normalized inflammation in wild-type mice depleted of CD20+ B cells and in Cd19/ mice. Remarkably, IL-10 production was restricted to this CD1dhiCD5+ B cell subset, with IL-10 production diminished in Cd19-/- mice, yet increased in hCD19Tg mice. Thereby, CD1dhiCD5+ B cells represent a unique subset of potent regulatory B cells.
全文地址:http://www.sciencedirect.com/science/article/pii/S1074761308001933
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