T regulatory cells and B cells cooperate to form a regulatory loop that maintains gut homeostasis and suppresses dextran sulfate sodium-induced colitis.

Authors:
L Wang
L Wang
National Pingtung University of Science and Technology
Taiwan
A Ray
A Ray
University of Utah
United States
X Jiang
X Jiang
School of Medicine
China
S Basu
S Basu
Banaras Hindu University
India
X Liu
X Liu
West China Hospital of Sichuan University
T Qian
T Qian
College of Medicine
R He
R He
Zhejiang University
China

Mucosal Immunol 2015 Nov 25;8(6):1297-312. Epub 2015 Mar 25.

Department of Immunology and Key Laboratory of Medical Molecular Virology of MOE/MOH, School of Basic Medical Sciences, Biotherapy Research Center of Fudan University, Shanghai, People's Republic of China.

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 that B cells and Tregs interact and cooperate to prevent excessive immune responses that can lead to colitis.

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http://dx.doi.org/10.1038/mi.2015.20DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4583327PMC

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November 2015
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