Pearse R N, Kawabe T, Bolland S, Guinamard R, Kurosaki T, Ravetch J V
Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, New York 10021, USA.
Immunity. 1999 Jun;10(6):753-60. doi: 10.1016/s1074-7613(00)80074-6.
Fc gammaRIIB is an inhibitory receptor that terminates activation signals initiated by antigen cross-linking of the BCR through the recruitment of SHIP. Fc gammaRIIB can also signal independently of BCR coligation to directly mediate an apoptotic response, requiring only an intact transmembrane domain. Failure to recruit SHIP, either by deletion of SHIP or mutation of Fc gammaRIIB, results in enhanced Fc gammaRIIB-triggered apoptosis. Thus, in the germinal center, where ICs are retained by FDCs, Fc gammaRIIB may be an active determinant in the negative selection of B cells whose BCRs have reduced affinity for antigen as a result of somatic hypermutation. Selection of B cells may represent the sum of opposing signals generated by the interaction of ICs with the BCR and Fc gammaRIIB through pathways modulated by SHIP.
FcγRIIB是一种抑制性受体，它通过募集SHIP来终止由BCR的抗原交联引发的激活信号。FcγRIIB也可以独立于BCR共结合发出信号，直接介导凋亡反应，这仅需要完整的跨膜结构域。通过缺失SHIP或FcγRIIB突变而未能募集SHIP，会导致FcγRIIB触发的凋亡增强。因此，在生发中心，免疫复合物被滤泡树突细胞保留，FcγRIIB可能是对那些由于体细胞高频突变而使其BCR对抗原亲和力降低的B细胞进行阴性选择的一个活跃决定因素。B细胞的选择可能代表了免疫复合物通过SHIP调节的途径与BCR和FcγRIIB相互作用所产生的相反信号的总和。
