Fearon D T
Wellcome Trust Immunology Unit, University of Cambridge School of Clinical Medicine, Hills Road, Cambridge, CB2 2SP, UK.
Semin Immunol. 1998 Oct;10(5):355-61. doi: 10.1006/smim.1998.0137.
The complement system covalently attaches C3d to microbial antigens which binds to CR2 on B lymphocytes, leading to a markedly enhanced adaptive immune response to that antigen. The enhancement is mediated by the cross-linking of the CR2-CD19 complex to mIg which augments the activation of several intracellular signalling pathways. Two additional receptors of the B lymphocyte, FcgammaRIIB and CD22, have opposing effects when cross-linked to mIg, the former suppressing signalling by recruiting the inositol phosphatase, SHIP, and the latter by activating the phosphotyrosine phosphatase, SHP-1. Two principles emerge from these studies: innate immunity guides the adaptive immune response, and activation of the B lymphocyte is determined by co-receptors which evaluate the biological characteristics of antigen.
补体系统将C3d共价连接到微生物抗原上,C3d与B淋巴细胞上的CR2结合,从而导致针对该抗原的适应性免疫反应显著增强。这种增强是由CR2-CD19复合物与mIg交联介导的,mIg可增强几种细胞内信号通路的激活。B淋巴细胞的另外两个受体FcγRIIB和CD22与mIg交联时具有相反的作用,前者通过招募肌醇磷酸酶SHIP抑制信号传导,后者通过激活磷酸酪氨酸磷酸酶SHP-1抑制信号传导。这些研究得出了两条原则:先天免疫指导适应性免疫反应,B淋巴细胞的激活由评估抗原生物学特性的共受体决定。