Centre for Inflammatory Diseases, Department of Medicine, Southern Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Vic., Australia.
Cell Mol Immunol. 2013 Sep;10(5):379-82. doi: 10.1038/cmi.2013.35. Epub 2013 Aug 12.
T-cell regulation by CD52-expressing CD4 T cells appears to operate by two different and possibly synergistic mechanisms. The first is by its release from the cell surface of CD4 T cells that express high levels of CD52 that then binds to the inhibitory sialic acid-binding immunoglobulin-like lectins-10 (Siglec-10) receptor to attenuate effector T-cell activation by impairing phosphorylation of T-cell receptor associated lck and zap-70. The second mechanism appears to be by crosslinkage of the CD52 molecules by an as yet unidentified endogenous ligand that is mimicked by a bivalent anti-CD52 antibody that results in their expansion.
表达 CD52 的 CD4 T 细胞对 T 细胞的调节似乎通过两种不同的、可能协同的机制起作用。第一种机制是通过表达高水平 CD52 的 CD4 T 细胞从细胞表面释放出来,然后与抑制性唾液酸结合免疫球蛋白样凝集素-10(Siglec-10)受体结合,通过削弱 T 细胞受体相关 lck 和 zap-70 的磷酸化来减弱效应 T 细胞的激活。第二种机制似乎是通过未鉴定的内源性配体交联 CD52 分子,这种配体被二价抗 CD52 抗体模拟,导致其扩增。