Emerging pathways of non-genomic glucocorticoid (GC) signalling in T cells

被引:59
作者
Boldizsar, Ferenc [1 ]
Talaber, Gergely [1 ]
Szabo, Mariann [1 ]
Bartis, Domokos [1 ]
Palinkas, Laszlo [1 ]
Nemeth, Peter [1 ]
Berki, Timea [1 ]
机构
[1] Univ Pecs, Dept Immunol & Biotechnol, Fac Med, H-7624 Pecs, Hungary
关键词
Glucocorticoid hormone; Mitochondrion; Non-genomic effects; T cell; ZAP-70; CHRONIC LYMPHOCYTIC-LEUKEMIA; A-STIMULATED THYMOCYTES; BLOOD MONONUCLEAR-CELLS; MEMBRANE LIPID MOBILITY; INDUCED APOPTOSIS; STEROID-HORMONES; OXIDATIVE-PHOSPHORYLATION; HSP90-SPECIFIC INHIBITOR; DOUBLE SUPRARENALECTOMY; AMPHIBIAN BRAIN;
D O I
10.1016/j.imbio.2009.10.003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In the last decade new glucocorticoid (GC)-signalling mechanisms have emerged. The evolving field of non-genomic GC actions was precipitated from two major directions: (i) some rapid/acute clinical GC applications could not be explained based on the relatively slowly appearing genomic GC action and (ii) accumulating evidence came to light about the discrepancy in the apoptosis sensitivity and GR expression of thymocytes and other lymphoid cell types. Herein, we attempt to sample the latest information in the field of non-genomic GC signalling in T cells, and correlate it with results from our laboratory. We discuss some aspects of the regulation of thymocyte apoptosis by GCs, paying special interest to the potential role(s) of mitochondrial GR signalling. The interplay between the T cell receptor (TcR) and glucocorticoid receptor (GR) signalling pathways is described in more detail, focusing on ZAP-70, which is a novel target of rapid GC action. (C) 2009 Elsevier GmbH. All rights reserved.
引用
收藏
页码:521 / 526
页数:6
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