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The imperfect control of self-reactive germinal center B cells


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.

Type Journal
Authors Brink, R.
Responsible Garvan Author Prof Robert Brink
Published Date 2014-03-29
Published Volume 28
Published Pages 97-101
Status Published in-print
DOI 10.1016/j.coi.2014.03.001
URL link to publisher's version
OpenAccess link to author's accepted manuscript version