DiPaolo Richard J, Glass Deborah D, Bijwaard Karen E, Shevach Ethan M
Section of Cellular Immunology, Laboratory of Immunology, National Institutes of Health, Bethesda, MD 20892-1892, USA.
J Immunol. 2005 Dec 1;175(11):7135-42. doi: 10.4049/jimmunol.175.11.7135.
Thymic-derived, naturally occurring, CD4+CD25+ regulatory T cells (nTreg) are potent suppressors of immune responses. A detailed understanding of which components of the development and activation of pathogenic effector T cells are inhibited by nTreg during the course of T cell-mediated, organ-specific autoimmunity is as yet unknown. We have analyzed the effects of polyclonal nTreg on the development of autoimmune gastritis. The nTreg inhibited the development of disease, but failed to inhibit the migration of effector cells into the gastric lymph node or stomach. Notably, nTreg did not inhibit the expansion of autoreactive T cells in the gastric lymph node. The primary effect of nTreg appeared to be inhibition of differentiation of autoantigen-specific T cells to Th1 effector cells, as reflected by a decrease in Ag-stimulated IFN-gamma production and a reduction in T-bet expression.
胸腺来源的天然存在的CD4+CD25+调节性T细胞（nTreg）是免疫反应的强效抑制因子。在T细胞介导的器官特异性自身免疫过程中，nTreg对致病性效应T细胞发育和激活的哪些成分具有抑制作用，目前尚不清楚。我们分析了多克隆nTreg对自身免疫性胃炎发展的影响。nTreg抑制了疾病的发展，但未能抑制效应细胞向胃淋巴结或胃的迁移。值得注意的是，nTreg并未抑制胃淋巴结中自身反应性T细胞的扩增。nTreg的主要作用似乎是抑制自身抗原特异性T细胞向Th1效应细胞的分化，这表现为抗原刺激的IFN-γ产生减少以及T-bet表达降低。
