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Impaired removal of V β8 + lymphocytes aggravates colitis in mice deficient for B cell lymphoma‐2‐interacting mediator of cell death ( Bim )
Author(s) -
Leucht K.,
Caj M.,
Fried M.,
Rogler G.,
Hausmann M.
Publication year - 2013
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/cei.12137
Subject(s) - colitis , mediator , immunology , lymphocyte , lymphoma , inflammation , apoptosis , biology , medicine , cancer research , endocrinology , biochemistry
Summary We investigated the role of B cell lymphoma ( BCL) ‐2‐interacting mediator of cell death ( Bim ) for lymphocyte homeostasis in intestinal mucosa. Lymphocytes lacking Bim are refractory to apoptosis. Chronic colitis was induced in B im ‐deficient mice ( B im –/– ) with dextran sulphate sodium ( DSS ). Weight loss and colonoscopic score were increased significantly in B im –/– mice compared to wild‐type mice. As Bim is induced for the killing of autoreactive cells we determined the role of Bim in the regulation of lymphocyte survival at mucosal sites. Upon chronic dextran sulphate sodium ( DSS) ‐induced colitis, B im –/– animals exhibited an increased infiltrate of lymphocytes into the mucosa compared to wild‐type mice. The number of autoreactive T cell receptor ( TCR) V β8 + lymphocytes was significantly higher in B im –/– mice compared to wild‐type controls. Impaired removal of autoreactive lymphocytes in B im –/– mice upon chronic DSS ‐induced colitis may therefore contribute to aggravated mucosal inflammation.

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