Frontiers in Immunology (Nov 2021)

Intestinal CD11b+ B Cells Ameliorate Colitis by Secreting Immunoglobulin A

  • Ying Fu,
  • Zhiming Wang,
  • Baichao Yu,
  • Yuli Lin,
  • Enyu Huang,
  • Enyu Huang,
  • Ronghua Liu,
  • Chujun Zhao,
  • Mingfang Lu,
  • Wei Xu,
  • Hongchun Liu,
  • Yongzhong Liu,
  • Luman Wang,
  • Luman Wang,
  • Yiwei Chu,
  • Yiwei Chu

DOI
https://doi.org/10.3389/fimmu.2021.697725
Journal volume & issue
Vol. 12

Abstract

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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.

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