Verkoczy Laurent K, Mårtensson Annica S, Nemazee David
Department of Immunology, The Scripps Research Institute, Mail Drop IMM-29, 10550 North Torrey Pines Road, La Jolla, California 92037, USA.
Curr Opin Immunol. 2004 Dec;16(6):808-14. doi: 10.1016/j.coi.2004.09.017.
Random assembly of antibody variable (V), diversity (D) and joining (J) gene segments creates a vast repertoire of antigen receptors, including autoreactive ones. Three ways that are known to reduce autoreactivity in the B-cell compartment include clonal deletion, functional inactivation and receptor editing, a mechanism involving a change in antigen receptor specificity through continued V(D)J recombination. New data suggest that editing can efficiently eliminate autoreactivity, yet, in an autoimmune context, secondary antibody gene rearrangements might also contribute to autoimmunity.
抗体可变区（V）、多样性区（D）和连接区（J）基因片段的随机组装产生了大量的抗原受体，包括自身反应性受体。已知在B细胞区室中减少自身反应性的三种方式包括克隆清除、功能失活和受体编辑，受体编辑是一种通过持续的V（D）J重组改变抗原受体特异性的机制。新数据表明，编辑可以有效地消除自身反应性，然而，在自身免疫的情况下，二次抗体基因重排也可能导致自身免疫。
