糖皮质激素诱导肿瘤坏死因子受体（GITR）-糖皮质激素诱导肿瘤坏死因子受体配体（GITRL）相互作用：共刺激还是对调节活性的反抑制作用？
The GITR-GITRL interaction: co-stimulation or contrasuppression of regulatory activity?
作者信息
Shevach Ethan M, Stephens Geoffrey L
机构信息
Cellular Immunology Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
出版信息
Nat Rev Immunol. 2006 Aug;6(8):613-8. doi: 10.1038/nri1867.
Stimulation of T cells through GITR (glucocorticoid-induced tumour-necrosis-factor-receptor-related protein) has been shown to enhance immunity to tumours and viral pathogens, and to exacerbate autoimmune disease. The effects of stimulation through GITR are generally thought to be caused by attenuation of the effector activity of immunosuppressive CD4+ CD25+ regulatory T (T(Reg)) cells. Here we propose a model in which GITR-GITR-ligand interactions co-stimulate both responder T-cell functions and the suppressive functions of T(Reg) cells.
通过糖皮质激素诱导的肿瘤坏死因子受体相关蛋白（GITR）刺激T细胞已被证明可增强对肿瘤和病毒病原体的免疫力，并加剧自身免疫性疾病。通常认为，通过GITR刺激产生的效应是由免疫抑制性CD4+CD25+调节性T（T(Reg)）细胞效应活性的减弱引起的。在此，我们提出一种模型，其中GITR与GITR配体的相互作用共同刺激应答性T细胞功能和T(Reg)细胞的抑制功能。
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