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在缺乏信号转导和转录激活因子1（STAT1）的情况下，CD4+ CD25+调节性T细胞发育受损：自身免疫性疾病易感性增加。

Impaired development of CD4+ CD25+ regulatory T cells in the absence of STAT1: increased susceptibility to autoimmune disease.

作者信息

Nishibori Takeaki, Tanabe Yoshinari, Su Leon, David Michael

机构信息

Department of Biology, University of California San Diego, Bonner Hall 3138, 9500 Gilman Drive, La Jolla, CA 92093, USA.

出版信息

J Exp Med. 2004 Jan 5;199(1):25-34. doi: 10.1084/jem.20020509. Epub 2003 Dec 29.

DOI:10.1084/jem.20020509
PMID:14699080
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1193645/
Abstract

Type I and II interferons (IFNs) exert opposing effects on the progression of multiple sclerosis, even though both IFNs use the signal transducer and activator of transcription 1 (STAT1) as a signaling mediator. Here we report that STAT1-deficient mice expressing a transgenic T cell receptor against myelin basic protein spontaneously develop experimental autoimmune encephalomyelitis with dramatically increased frequency. The heightened susceptibility to this autoimmune disease appears to be triggered by a reduced number as well as a functional impairment of the CD4+ CD25+ regulatory T cells in STAT1-deficient animals. Adoptive transfer of wild-type regulatory T cells into STAT1-deficient hosts is sufficient to prevent the development of autoimmune disease. These results demonstrate an essential role of STAT1 in the maintenance of immunological self-tolerance.

摘要

I型和II型干扰素（IFN）对多发性硬化症的进展具有相反的作用，尽管这两种干扰素都将信号转导子和转录激活子1（STAT1）用作信号传导介质。在此我们报告，表达针对髓鞘碱性蛋白的转基因T细胞受体的STAT1缺陷小鼠会自发发生实验性自身免疫性脑脊髓炎，且发病频率显著增加。STAT1缺陷动物对这种自身免疫性疾病易感性的增加似乎是由CD4+ CD25+调节性T细胞数量减少以及功能受损所触发的。将野生型调节性T细胞过继转移到STAT1缺陷宿主中足以预防自身免疫性疾病的发生。这些结果证明了STAT1在维持免疫自身耐受性中的重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/4a1978069890/20020509f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/eb3f28202006/20020509f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/a8e9b76e19a4/20020509f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/00a40d7b6cc4/20020509f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/997aba09b13c/20020509f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/86b72e7ed54e/20020509f6ab.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/4a1978069890/20020509f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/eb3f28202006/20020509f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/dab55b3a3b75/20020509f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/a8e9b76e19a4/20020509f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/00a40d7b6cc4/20020509f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/997aba09b13c/20020509f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/86b72e7ed54e/20020509f6ab.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c12d/1887721/4a1978069890/20020509f7.jpg

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