期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 203, 期 3, 页码 731-741出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20051407
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资金
- NIAID NIH HHS [R01 AI018785, AI52225, P01 AI022295, R01 AI052225, AI-17134, AI-18785, R56 AI017134, R37 AI018785, R01 AI017134, R56 AI018785, AI-22295] Funding Source: Medline
Although B cells that respond with high avidity to self-antigen are eliminated early in their development, many autoreactive B cells escape elimination and are tolerized later in their lives via anergy. Anergic B cells are unresponsive to antigen and die prematurely. It has been suggested that the proapoptotic protein, Bim, controls the fate of anergic B cells. To test this idea, mice lacking Bim were crossed with mice that express soluble hen egg lysozyme and whose B cells bear receptors specific for the protein. In Bim(+/+) mice these B cells are anergic and die rapidly. If the mice lack Bim, however, the B cells live longer, are more mature, respond to antigen, and secrete anti-hen egg lysozyme antibodies. This break of tolerance is not due to expression of endogenous B cell receptors, nor is it dependent on T cells. Rather, it appears to be due to a reduced requirement for the cytokine BAFF. Normal B cells require BAFF both for differentiation and survival. Bim(-/-) B cells, on the other hand, require BAFF only for differentiation. Therefore, autoreactive B cells are allowed to survive if they lack Bim and thus accumulate sufficient signals from differentiating factors to drive their maturation and production of autoantibodies.
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