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Curr Opin Immunol. 2014 Jun;28:97-101. doi: 10.1016/j.coi.2014.03.001. Epub 2014 Mar 28.

The imperfect control of self-reactive germinal center B cells.

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Immunology Division, Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia; St Vincent's Clinical School, UNSW Australia, Darlinghurst, NSW 2010, Australia. Electronic address:


Unlike T cells, B cells diversify their antigen receptor (BCR) binding specificities at two distinct stages of differentiation. Thus, in addition to initial variable region gene rearrangements, B cells recruited into T-dependent immune responses further modify their BCR specificity via iterative rounds of somatic hypermutation (SHM) within germinal centers (GCs). Although critical for providing the high-affinity antibody specificities required for long-term immune protection, SHM can also generate self-reactive B cells capable of differentiating into autoantibody-producing plasma cells. Recent data confirm that self-reactive GC B cells can be effectively removed from the secondary repertoire so as to maintain self-tolerance. However, they can also escape deletion under certain circumstances and so contribute to autoimmune disease via production of somatically mutated, pathogenic autoantibodies.

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