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Summary
Immunity to pathogens and tolerance to self are cardinal features of immune systems. Immunological specificity is encoded by receptors expressed on the surface of lymphocytes that are generated through random assembly of variable, diversity, and joining (VDJ) gene segments during B and T lymphocyte development. In addition, B lymphocytes further diversify this initial repertoire through somatic hypermutation of antibody genes in germinal centers (transient structures that form in lymphoid organs in which high-affinity antibodies arise). On page 223 of this issue, Burnett et al. (1) devise a strategy to track the fate of self-reactive B cells in germinal centers elicited by a foreign antigen that structurally mimics a self-antigen (antigen mimicry). The authors provide evidence that hypermutation of antibody genes in germinal centers can repair self-reactive antibodies. These results have implications for how broadly neutralizing antibodies to HIV-1 may be formed.
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