[PDF][PDF] SHIP recruitment attenuates FcγRIIB-induced B cell apoptosis
RN Pearse, T Kawabe, S Bolland, R Guinamard… - Immunity, 1999 - cell.com
RN Pearse, T Kawabe, S Bolland, R Guinamard, T Kurosaki, JV Ravetch
Immunity, 1999•cell.comFcγRIIB is an inhibitory receptor that terminates activation signals initiated by antigen cross-
linking of the BCR through the recruitment of SHIP. FcγRIIB 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
FcγRIIB, results in enhanced FcγRIIB-triggered apoptosis. Thus, in the germinal center,
where ICs are retained by FDCs, FcγRIIB may be an active determinant in the negative …
linking of the BCR through the recruitment of SHIP. FcγRIIB 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
FcγRIIB, results in enhanced FcγRIIB-triggered apoptosis. Thus, in the germinal center,
where ICs are retained by FDCs, FcγRIIB may be an active determinant in the negative …
Abstract
FcγRIIB is an inhibitory receptor that terminates activation signals initiated by antigen cross-linking of the BCR through the recruitment of SHIP. FcγRIIB 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 FcγRIIB, results in enhanced FcγRIIB-triggered apoptosis. Thus, in the germinal center, where ICs are retained by FDCs, FcγRIIB 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 FcγRIIB through pathways modulated by SHIP.
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