B10 cells and regulatory B cells balance immune responses during inflammation, autoimmunity, and cancer
The ability of B cells to negatively regulate cellular immune responses and inflammation has only recently been described. Hallmark papers from a number of distinguished laboratories have identified phenotypically diverse B‐cell subsets with regulatory functions during distinct autoimmune diseases,...
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Published in | Annals of the New York Academy of Sciences Vol. 1183; no. 1; pp. 38 - 57 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Malden, USA
Blackwell Publishing Inc
01.01.2010
Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
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Summary: | The ability of B cells to negatively regulate cellular immune responses and inflammation has only recently been described. Hallmark papers from a number of distinguished laboratories have identified phenotypically diverse B‐cell subsets with regulatory functions during distinct autoimmune diseases, including IL‐10‐producing B cells, CD5+ B‐1a cells, CD1d+ marginal zone B cells, and transitional‐2‐marginal zone precursor B cells. Most recently, a numerically rare and phenotypically unique CD1dhiCD5+CD19hi subset of regulatory B cells has been identified in the spleens of both normal and autoimmune mice. CD1dhiCD5+ B cells with the capacity to produce IL‐10 have been named B10 cells as they produce IL‐10 exclusively and are the predominant B‐cell source of IL‐10. Remarkably, B10 cells are potent negative regulators of inflammation and autoimmunity in mouse models of disease in vivo. Herein, our current understanding of B10‐cell development and function is reviewed in the context of previous studies that have identified and characterized regulatory B cells, emerging evidence for B10‐cell regulation of tumor immunity, and the likelihood that B10 cells exist in humans. |
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Bibliography: | ArticleID:NYAS5137 istex:F58539791F405DA372765577FBDC6751FC15CAE9 ark:/67375/WNG-M10DVFSF-M ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 ObjectType-Feature-1 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0077-8923 1749-6632 |
DOI: | 10.1111/j.1749-6632.2009.05137.x |