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Mannose‐capped lipoarabinomannan‐induced B10 cells decrease severity of dextran sodium sulphate‐induced inflammatory bowel disease in mice
Author(s) -
Yuan Chun-Hui,
Li Xin,
Luo Liang,
Wang Ya-Ping,
Zhang Dong-Li,
Zhou KaiLiang,
Zhang XiaoLian,
Pan Qin
Publication year - 2020
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12843
Subject(s) - lipoarabinomannan , inflammatory bowel disease , immunology , medicine , mesenteric lymph nodes , pathogenesis , ulcerative colitis , colitis , spleen , pathology , disease , tuberculosis , mycobacterium tuberculosis
Inflammatory bowel disease (IBD) is a chronic, non‐specific, inflammatory gastrointestinal disease that mainly consists of Crohn's disease and ulcerative colitis. However, the aetiology and pathogenesis of IBD are still unclear. B10 (IL‐10 producing regulatory B) cells, a subset of regulatory B cells, are known to contribute to intestinal homeostasis and the aberrant frequency of B10 cells is associated with IBD. We have recently reported that B10 cells can be induced by ManLAM (mannose‐capped lipoarabinomannan), a major cell‐wall lipoglycan of M tb ( Mycobacterium tuberculosis ). In the current study, the ManLAM‐induced B10 cells were adoptively transferred into IL(interleukin)‐10 −/− mice and the roles of ManLAM‐induced B10 cells were investigated in DSS (dextran sodium sulphate)‐induced IBD model. ManLAM‐induced B10 cells decrease colitis severity in the mice. The B10 cells downregulate Th1 polarization in spleen and MLNs (mesenteric lymph nodes) of DSS‐treated mice. These results suggest that IL‐10 production by ManLAM‐treated B cells contributes to keeping the balance between CD4 + T cell subsets and protect mice from DSS‐induced IBD.