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Peyer's patches-derived CD11b+ B cells recruit regulatory T cells through CXCL9 in dextran sulphate sodium-induced colitis.

Immunology. 2018 Nov;155(3):356-366. doi:10.1111/imm.12977. Epub 2018 Jul 26
Zhiming Wang 1 , Hushan Zhang 1 , Ronghua Liu 1 , Tingting Qian 1 , Jiajing Liu 1 , Enyu Huang 2 , Zhou Lu 1 , Chujun Zhao 3 , Luman Wang 4 , Yiwei Chu 4
Zhiming Wang 1 , Hushan Zhang 1 , Ronghua Liu 1 , Tingting Qian 1 , Jiajing Liu 1 , Enyu Huang 2 , Zhou Lu 1 , Chujun Zhao 3 , Luman Wang 4 , Yiwei Chu 4
+ et al

[No authors listed]

Author information
  • 1 Department of Immunology, School of Basic Medical Sciences, Institute of Biomedical Sciences, Fudan University, Shanghai, China.
  • 2 Department of Pathology, The University of Hong Kong, Hong Kong, China.
  • 3 Northfield Mount Hermon School, Mount Hermon, MA, USA.
  • 4 Biotherapy Research Centre, Fudan University, Shanghai, China.

摘要


Regulatory T (Treg) cells play an essential role in the maintenance of intestinal homeostasis. In Peyer's patches (PPs), which comprise the most important IgA induction site in the gut-associated lymphoid tissue, Treg cells promote IgA isotype switching. However, the mechanisms underlying their entry into PPs and isotype switching facilitation in activated B cells remain unknown. This study, based on the dextran sulphate sodium (DSS)-induced colitis model, revealed that Treg cells are significantly increased in PPs, along with CD11b+ B-cell induction. Immunofluorescence staining showed that infiltrated Treg cells were located around CD11b+ B cells and produced transforming growth factor-β, thereby inducing IgA+ B cells. Furthermore, in vivo and in vitro studies revealed that CD11b+ B cells in PPs had the capacity to recruit Treg cells into PPs rather than promoting their proliferation. Finally, we found that Treg cell recruitment was mediated by the chemokine CXCL9 derived from CD11b+ B cells in PPs. These findings demonstrate that CD11b+ B cells induced in PPs during colitis actively recruit Treg cells to accomplish IgA isotype switch in a CXCL9-dependent manner.

KEYWORDS: CD11b+ B cells, colitis, regulatory T cells