Immune regulation by CD52-expressing CD4 T cells

被引:18
作者
Toh, Ban-Hock [1 ]
Kyaw, Tin [1 ,2 ]
Tipping, Peter [1 ]
Bobik, Alex [2 ]
机构
[1] Monash Univ, Fac Med Nursing & Hlth Sci, Southern Clin Sch, Ctr Inflammatory Dis,Dept Med, Clayton, Vic, Australia
[2] Baker IDI Heart & Diabet Inst, Vasc Biol & Atherosclerosis Lab, Melbourne, Vic, Australia
关键词
MULTIPLE-SCLEROSIS; AUTOIMMUNE-DISEASES; CD52; ANTIGEN; 4C8; ALEMTUZUMAB; EXPRESSION; SIGLEC-10; TRANSPLANTATION; INDUCTION; CAMPATH-1;
D O I
10.1038/cmi.2013.35
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:379 / 382
页数:4
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