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Self-reactive B cells are eliminated in a series of checkpoints that are triggered by antigen binding. Recent reports have shown that in addition to the processes of elimination at the immature B-cell stage, B-cell anergy and regulation of T-cell help, self-reactive cells are also controlled by follicular competition, Fas-mediated elimination by T cells and censoring in the germinal centres. Each checkpoint operates at a threshold that reflects the need to maintain immune diversity at the same time as suppressing autoimmune disease. Analysis of the motheaten mutation has given a direct demonstration of how such thresholds can be modulated by genetic effects.


Journal article


Curr Opin Immunol

Publication Date





804 - 811


Animals, Autoimmunity, B-Lymphocytes, Germinal Center, Humans, Immune Tolerance, Lymphocyte Activation, Mice, Mice, Transgenic, Models, Immunological, Spleen, fas Receptor