Suppr超能文献

通过长期暴露于外源性超抗原在体内对成熟T细胞进行深度缺失。

Profound deletion of mature T cells in vivo by chronic exposure to exogenous superantigen.

作者信息

McCormack J E, Callahan J E, Kappler J, Marrack P C

机构信息

Howard Hughes Medical Institute, Denver, CO.

出版信息

J Immunol. 1993 May 1;150(9):3785-92.

PMID:8473733
Abstract

It has been noted previously that superantigens can under different circumstances stimulate activation, expansion, anergy, and/or deletion of reactive T cells in vivo and in vitro. Here, we present a detailed examination of the expansion and deletion of T cells in vivo in response to the superantigens staphylococcal enterotoxin A (SEA) in the B10.BR mouse. Mice were either acutely or chronically exposed to varying doses of SEA, and the relative level of T cells bearing SEA-reactive V beta elements was followed over time in lymphocytes purified from peripheral blood, lymph nodes, mesenteric lymph nodes, and spleen. In most cases, an initial sharp rise in the proportion of reactive T cells was followed by a dramatic decline. Cells of the CD4+ and CD8+ lineages displayed subtle differences in their kinetics of activation and deletion, as well as their sensitivity to different doses of SEA. Furthermore, cells bearing either of two V beta elements previously characterized as SEA-reactive showed some differences in their responses to SEA treatment. Acute exposure usually caused the disappearance of only 50% to 70% of reactive T cells; however, chronic exposure to SEA caused almost complete deletion of target T cells. Deletion was evident even in animals treated with very low doses of SEA, doses that were too small to cause any apparent T cell proliferation. Thus, proliferation does not appear to be a prerequisite for peripheral deletion of T cells.

摘要

先前已经注意到,超抗原在不同情况下可在体内和体外刺激反应性T细胞的激活、扩增、无反应性和/或缺失。在此,我们详细研究了B10.BR小鼠体内T细胞对超抗原葡萄球菌肠毒素A(SEA)的反应,观察其扩增和缺失情况。小鼠急性或慢性暴露于不同剂量的SEA,随后在从外周血、淋巴结、肠系膜淋巴结和脾脏中纯化的淋巴细胞中,跟踪携带SEA反应性Vβ元件的T细胞的相对水平随时间的变化。在大多数情况下,反应性T细胞比例最初急剧上升,随后急剧下降。CD4+和CD8+谱系的细胞在激活和缺失动力学以及对不同剂量SEA的敏感性方面表现出细微差异。此外,携带先前被鉴定为SEA反应性的两种Vβ元件之一的细胞,对SEA处理的反应也存在一些差异。急性暴露通常仅导致50%至70%的反应性T细胞消失;然而,慢性暴露于SEA会导致靶T细胞几乎完全缺失。即使在用非常低剂量SEA处理的动物中也明显出现缺失,这些剂量太小以至于不会引起任何明显的T细胞增殖。因此,增殖似乎不是T细胞外周缺失的先决条件。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验