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在氯化汞诱导的系统性自身免疫中,T淋巴细胞表面淋巴细胞功能相关抗原-1(LFA-1)、细胞间黏附分子-1(ICAM-1)以及肿瘤坏死因子受体家族成员OX40的表达增强。

Enhanced T lymphocyte expression of LFA-1, ICAM-1, and the TNF receptor family member OX40 in HgCl2-induced systemic autoimmunity.

作者信息

Roos A, Claessen N, Weening J J, Aten J

机构信息

Department of Pathology, University of Amsterdam, The Netherlands.

出版信息

Scand J Immunol. 1996 May;43(5):507-18. doi: 10.1046/j.1365-3083.1996.d01-66.x.

DOI:10.1046/j.1365-3083.1996.d01-66.x
PMID:8633208
Abstract

Injection of mercuric chloride into Brown Norway (BN) rats induces a T lymphocyte-dependent autoimmune syndrome. In order to investigate whether modification of adhesion and costimulatory molecules on T lymphocytes may be involved in early T lymphocyte activation by HgCl2, the authors analysed expression of these molecules in peripheral lymph node cells from BN rats at day 4 after injection of HgCl2. Tri-colour flow cytometry was performed for expression analysis within CD45RC-defined subsets of CD4+ and CD8+ cells. Compared to control rats, HgCl2-exposed rats showed increased numbers of lymphocytes, especially of T lymphocyte blast cells. The levels of LFA-1 expression as well as the fractions of ICAM-1 + cells were significantly increased in all CD45RC-defined subsets of CD4+ and CD8+ cells. Within the CD4 + CD45RC10 T lymphocyte population, HgCl2-injected rats showed a highly significant increase in the number of cells expressing OX40, which is a member of the TNF receptor family. Moreover, only CD4 + CD45RC10 blast cells of HgCl2-exposed rats showed decreased expression of CD43, increased expression of CD49d and decreased numbers of CD26 + cells. The results indicate that induction of autoimmunity by HgCl2 in BN rats is associated with altered expression of T lymphocyte costimulatory molecules, predominantly on CD4+ CD45RC10 cells, which may be caused by a direct effect of HgCl2 on these cells, and may precipitate further activation of T and B lymphocytes by HgCl2.

摘要

向棕色挪威(BN)大鼠注射氯化汞会诱发一种T淋巴细胞依赖性自身免疫综合征。为了研究T淋巴细胞上黏附分子和共刺激分子的改变是否可能参与氯化汞对T淋巴细胞的早期激活,作者分析了注射氯化汞后第4天BN大鼠外周淋巴结细胞中这些分子的表达。采用三色流式细胞术对CD45RC定义的CD4⁺和CD8⁺细胞亚群进行表达分析。与对照大鼠相比,暴露于氯化汞的大鼠淋巴细胞数量增加,尤其是T淋巴细胞母细胞。在CD45RC定义的所有CD4⁺和CD8⁺细胞亚群中,LFA - 1表达水平以及ICAM - 1⁺细胞比例均显著增加。在CD4⁺CD45RC10 T淋巴细胞群体中,注射氯化汞的大鼠中表达OX40(肿瘤坏死因子受体家族成员)的细胞数量显著增加。此外,仅暴露于氯化汞的大鼠的CD4⁺CD45RC10母细胞显示CD43表达降低、CD49d表达增加以及CD26⁺细胞数量减少。结果表明氯化汞在BN大鼠中诱导自身免疫与T淋巴细胞共刺激分子表达改变有关,主要发生在CD4⁺CD45RC10细胞上,这可能是氯化汞对这些细胞的直接作用所致,并且可能促使氯化汞进一步激活T和B淋巴细胞。

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Enhanced T lymphocyte expression of LFA-1, ICAM-1, and the TNF receptor family member OX40 in HgCl2-induced systemic autoimmunity.在氯化汞诱导的系统性自身免疫中,T淋巴细胞表面淋巴细胞功能相关抗原-1(LFA-1)、细胞间黏附分子-1(ICAM-1)以及肿瘤坏死因子受体家族成员OX40的表达增强。
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