O'Rourke L, Tooze R, Fearon D T
Wellcome Trust Immunology Unit, University of Cambridge School of Clinical Medicine, Cambridge, CB2 2SP, UK.
Curr Opin Immunol. 1997 Jun;9(3):324-9. doi: 10.1016/s0952-7915(97)80077-5.
The past year has seen advances in our understanding of accessory membrane proteins that modulate the B cell response to antigen-receptor stimulation. The generation of complement receptor deficient mice has reinforced our appreciation of the importance of complement receptors in the B cell response to antigen. The association of inositol polyphosphate 5-phosphatase with FcgammaRIIB suggests another mechanism, in addition to recruitment of the phosphotyrosine phosphatase SHP-1, by which secreted immunoglobulin can limit further response to antigen. The in vivo function of CD22 in regulating the threshold of antigen-receptor signalling has been shown using CD22-deficient mice. Lastly, B cell receptor signalling in the B-1 subset of B lymphocytes has been demonstrated to be negatively regulated by CD5.
在过去的一年里,我们对调节B细胞对抗抗原受体刺激反应的辅助膜蛋白的理解取得了进展。补体受体缺陷小鼠的产生,加深了我们对补体受体在B细胞对抗抗原反应中重要性的认识。肌醇多磷酸5-磷酸酶与FcγRIIB的关联,表明除了募集磷酸酪氨酸磷酸酶SHP-1之外,分泌型免疫球蛋白还可通过另一种机制限制对抗抗原的进一步反应。利用CD22缺陷小鼠已证明CD22在体内调节抗原受体信号阈值的功能。最后,已证明B淋巴细胞B-1亚群中的B细胞受体信号传导受CD5负调控。