感染破坏了T细胞的耐受性
M Röcken1, J F Urban, E M Shevach
1Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.
Nature
|September 3, 1992
概括
感染Nippostrongylus brasiliensis可以破坏由Staphylococcus enterotoxin B (SEB) 建立的T细胞耐受性. 这表明传染剂可能通过激活无性T细胞引发自身免疫性疾病.
科学领域:
- 免疫学 免疫学 免疫学
- 这是一种自身免疫力.
- 传染性疾病 传染性疾病
背景情况:
- 通过克隆删除或无能性建立的T细胞耐受性,可以防止自身免疫反应.
- 自主反应性T细胞通常被抑制以保持自我耐受性.
研究的目的:
- 调查是否同时感染可以破坏已建立的T细胞耐受性.
- 确定传染病原体可能绕过T细胞耐受性的机制.
主要方法:
- 在小鼠中诱导T细胞耐受性,使用Staphylococcus enterotoxin B (SEB).
- 在实验室中与SEB挑战耐受性T细胞,以评估细胞因子 (互白素-2,互白素-4) 的产生.
- 用线虫Nippostrongylus brasiliensis感染耐受性小鼠,并在体内分析T细胞反应.
主要成果:
- 在体外SEB挑战时,耐受SEB的T细胞没有产生互白素-2或-4 .
- 在SEB耐受性小鼠中,N. brasiliensis感染导致了耐受性T细胞的正常扩张.
- 感染还导致SEB反应性,交白素-4生成的T细胞在耐受性和正常动物中增加.
结论:
- 尼波斯特朗吉勒斯巴西尼斯感染有效地规避了SEB诱导的T细胞耐受性.
- 传染病原体可以通过其他途径激活无性T细胞来启动自身免疫.
- 这项研究突出了自身免疫性疾病发展中的传染性触发因子的潜在机制.
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