FcgammaRII expression on follicular dendritic cells and immunoreceptor XXXX -based inhibition motif signaling in B cells.

@entity20305 @entity20216 @entity7110 @entity742 @entity19 @entity32891 @entity669
@entity7110 ( @entity7110 ) initiate immunoreceptor @entity669 -based inhibition motif (ITIM) signaling and inhibit B cell activation by coligating B cell receptor for antigen (BCR) and FcgammaRII. Nevertheless, @entity7110 on follicular dendritic cells (FDC) stimulate rapid @entity32891 cell proliferation suggesting that interactions between @entity7110 and FDC render @entity7110 capable of B cell activation. To understand this, we studied the kinetics of @entity20305 (CR1_2) expressions during the GC reaction and determined whether FDC FcgammaRII could bind Fc in @entity7110 and block ITIM signaling. @entity19 were immunized with @entity742 red blood cells (SRBC), and CR1_2 and FcgammaRII levels in FDC reticula were monitored. The role of FDC FcgammaRII was studied using anti-BCR-stimulated A20 cells. Levels of FDC FcgammaRII in spleens of SRBC-injected @entity19 increased within 24 h and were dramatically increased (approximately 50-fold) on days 3 and 5. In contrast, CR1_2 levels increased less than twofold. Addition of normal FDC, but not FDC lacking FcgammaRII, reduced and reversed anti-BCR-induced @entity20216 phosphorylation in A20 cells. FDC were able to induce normal recall responses even after overnight incubation of the lymphocytes with @entity7110 to stimulate ITIM signaling. Engagement of Ig Fc with numerous FcgammaRII on FDC appears to minimize @entity7110 -induced ITIM signaling. Thus, rapid up-regulation of FDC FcgammaRII may explain why poorly immunogenic @entity7110 are rendered highly immunogenic when presented by FDC in GC.
