Cornall R J, Goodnow C C, Cyster J G
Howard Hughes Medical Institute, Stanford University School of Medicine, California 94305, USA.
Curr Opin Immunol. 1995 Dec;7(6):804-11. doi: 10.1016/0952-7915(95)80052-2.
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.
