Intestinal CD11b + B Cells Ameliorate Colitis by Secreting Immunoglobulin A.

The intestinal mucosal immune environment requires multiple immune cells to maintain homeostasis. Although intestinal B cells are among the most important immune cells, little is known about the mechanism that they employ to regulate immune homeostasis. In this study, we found that CD11b ⁺ B cells significantly accumulated in the gut lamina propria and Peyer's patches in dextran sulfate sodium-induced colitis mouse models and patients with ulcerative colitis. Adoptive transfer of CD11b ⁺ B cells, but not CD11b ^-/- B cells, effectively ameliorated colitis and exhibited therapeutic effects. Furthermore, CD11b ⁺ B cells were found to produce higher levels of IgA than CD11b ^- B cells. CD11b deficiency in B cells dampened IgA production, resulting in the loss of their ability to ameliorate colitis. Mechanistically, CD11b ⁺ B cells expressed abundant TGF-β and TGF-β receptor II, as well as highly activate phosphorylated Smad2/3 signaling pathway, consequently promoting the class switch to IgA. Collectively, our findings demonstrate that CD11b ⁺ B cells are essential intestinal suppressive immune cells and the primary source of intestinal IgA, which plays an indispensable role in maintaining intestinal homeostasis.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2021 Fu, Wang, Yu, Lin, Huang, Liu, Zhao, Lu, Xu, Liu, Liu, Wang and Chu.)