The influence of complement receptor type 1 (CD35) and decay-accelerating factor (CD55) on complement receptor type 2- (CD21) mediated alternative pathway activation by B cells.
The influence of complement receptor type 1 (CR1; CD35) and decay-accelerating factor (DAF; CD55), both down-regulators of complement activation, on the complement receptor type 2- (CR2) mediated alternative pathway (AP) activation of complement on normal B cells, was assessed. The data indicate that, while neither DAF nor CR1 hinder the function of the AP convertase formed on CR2, CR1 plays a significant role in the remodelling of C3b fragments, generated by the convertase and deposited at secondary acceptor sites on the B-cell surface, such that they become suitable ligands for CR2. The significance of this finding is briefly discussed.
Leslie
R G
RG
Department of Immunology & Microbiology, Institute of Medical Biology, University of Southern Denmark, Denmark.
D001402:B-Lymphocytes / Q000276:immunology*; D018958:CD55 Antigens / Q000276:immunology*; D018929:Cell Culture Techniques; D003176:Complement C3 / Q000378:metabolism; D003170:Complement Pathway, Alternative / Q000276:immunology*; D006801:Humans; D017463:Receptors, Complement 3b / Q000276:immunology*; D017464:Receptors, Complement 3d / Q000276:immunology; D014407:Tumor Cells, Cultured
D018958:CD55 Antigens; D003176:Complement C3; D017463:Receptors, Complement 3b; D017464:Receptors, Complement 3d