期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 103, 期 1, 页码 153-158出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0509784103
关键词
allergy; IgE; immune regulation; Btk
资金
- NIAID NIH HHS [AI61796, R01 AI050209, R01 AI038348, AI51125, AI38348, R01 AI061796, AI50209] Funding Source: Medline
Btk plays crucial roles in the differentiation and activation of B and myeloid cells. Despite drastic reductions of other lg isotypes, paradoxically high IgE responses have been known in btk mutant mice. Here we show that btk(-/-) clendritic cells exhibit a more mature phenotype and a stronger in vitro and in vivo T cell-stimulatory ability than wild-type cells. Increased IgE responses were induced by adoptive transfer of btk(-/-) clendritic cells into mice. Consistent with the stronger T cell-stimulatory ability of btk(-/-) dendritic cells, btk(-/-) mice exhibited enhanced inflammation in Th2-driven asthma and Th1-driven contact sensitivity experiments. These negative regulatory functions of Btk in dendritic cells appear to be mediated mainly through autocrine secretion of IL-10 and subsequent activation of Stat3.
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