IL-2 and autoimmune disease

被引:52
作者
Schimpl, A [1 ]
Berberich, I [1 ]
Kneitz, B [1 ]
Krämer, S [1 ]
Santner-Nanan, B [1 ]
Wagner, S [1 ]
Wolf, M [1 ]
Hünig, T [1 ]
机构
[1] Univ Wurzburg, Inst Virol & Immunobiol, D-97078 Wurzburg, Germany
关键词
autoimmune disease; activation induced cell death; T cell growth factor; IL-2; deficiency;
D O I
10.1016/S1359-6101(02)00022-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A decade after the first description of IL-2-deficient mice, the redundancy of IL-2 as a T cell growth factor is well accepted and the focus of research has shifted to the unexpected multiorgan autoimmunity and inflammation observed in mice lacking components of the IL-2/IL-2R system. So far, a set of defects at the levels of repertoire selection, the generation of suppressive regulatory T cells, T cell homing and clonal contraction via activation induced cell death (AICD) have been documented. We propose that these individual defects jointly contribute to the severe disturbance of T cell homeostasis and self-tolerance underlying the immunopathology of the IL-2 deficiency syndrome. (C) 2002 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:369 / 378
页数:10
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