期刊
MUCOSAL IMMUNOLOGY
卷 8, 期 6, 页码 1297-1312出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2015.20
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资金
- National Institutes of Health [R01 AI069358, R56 AI106672-01]
- BloodCenter Research Foundation (BD)
- National Science Foundation of China [81273215, 91229110]
- National Basic Research Program of China (973 Programs) [2011CB910404]
- China Postdoctoral Science Foundation [2014M5502141]
- Specialized Research Fund for the Doctoral Program of Higher Education [20120071110046]
- Grants-in-Aid for Scientific Research [25460604] Funding Source: KAKEN
Regulatory T cells (Tregs) and B cells present in gut-associated lymphoid tissues (GALT) are both implicated in the resolution of colitis. However, how the functions of these cells are coordinated remains elusive. We used the dextran sulfate sodium (DSS)-induced colitis model combined with gene-modified mice to monitor the progression of colitis, and simultaneously examine the number of Tregs and B cells, and the production of IgA antibodies. We found that DSS-treated mice exhibited more severe colitis in the absence of B cells, and that the adoptive transfer of B cells attenuated the disease. Moreover, the transfer of IL-10(-/-) B cells also attenuated colitis, suggesting that B cells inhibited colitis through an interleukin-10 (IL-10)-independent pathway. Furthermore, antibody depletion of Tregs resulted in exacerbated colitis. Intriguingly, the number of GALT Tregs in B cell-deficient mice was significantly decreased during colitis and the adoptive transfer of B cells into these mice restored the Treg numbers, indicating that B cells contribute to Treg homeostasis. We also found that B cells induced the proliferation of Tregs that in turn promoted B-cell differentiation into IgA-producing plasma cells. These results demonstrate thatBcells and Tregs interact and cooperate to prevent excessive immune responses that can lead to colitis.
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