Coligation of the B cell receptor with complement receptor type 2 (CR2/CD21) using its natural ligand C3dg: activation without engagement of an inhibitory signaling pathway.

摘要: C3dg is a cleavage product of the C3 component complement that can facilitate coligation receptor 2 (CR2/CD21) with BCR via C3dg/Ag complexes. This interaction greatly amplify BCR-mediated signaling events and acts to lower threshold for B cell activation. Although previous studies have used anti-CR2 Abs or chimeric Ags in context transgenic mice as surrogate C3d-containing ligands, we physiological form C3d study cells from wild-type C57BL/6 mice. We find while CR2-enhanced causes intracellular Ca2+ mobilization total pTyr phosphorylation an intensity comparable optimal ligation using anti-IgM Abs, it does so limited activation inhibitory effectors (such CD22, Src homology region domain containing phosphatase 1, SHIP-1) without substantial cross-linking. In summary, demonstrate may proceed not only through previously described amplification positive pathways, but potentially augmented by lack normal inhibitory/feedback signaling.