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氯化汞诱导的小鼠全身性自身免疫疾病:对自身蛋白产生反应的辅助性T细胞

Murine systemic autoimmune disease induced by mercuric chloride: T helper cells reacting to self proteins.

作者信息

Kubicka-Muranyi M, Kremer J, Rottmann N, Lübben B, Albers R, Bloksma N, Lührmann R, Gleichmann E

机构信息

Division of Immunology, Heinrich Heine University Düsseldorf, Germany.

出版信息

Int Arch Allergy Immunol. 1996 Jan;109(1):11-20. doi: 10.1159/000237226.

DOI:10.1159/000237226
PMID:8527945
Abstract

HgCl2 induces a CD4+ T-cell-dependent systemic autoimmune disease in susceptible strains of rats and mice. In rats, autoreactive T cells were shown to be involved, whereas in mice, attention has focussed on the demonstration of 'Hg-specific' T cells. To clarify these seemingly different T cell involvements, T cells from B10.S mice treated with HgCl2 for 1 or 8 weeks were analyzed for their capacity to mount anamnestic responses against various self antigens (Ags) which either contained Hg or did not. T cells from donors short-term treated with HgCl2 failed to mount memory responses to Hg-free Ags, but mounted a significant response to HgCl2 and also reacted with Hg-containing self Ags. Interestingly, T cells from donors long-term treated with HgCl2 showed a different pattern of reactivity. They hardly reacted to HgCl2 and reacted poorly to Hg-containing splenic proteins, but responded vigorously to nuclei and fibrillarin irrespective of whether these self constituents had been treated with HgCl2 or not. Conceivably, the initial activation of T cells that recognize Hg in combination with nuclear self proteins, such as fibrillarin, eventually results in activation of T cells specific for the unaltered self proteins.

摘要

氯化汞在大鼠和小鼠的易感品系中可诱发一种依赖CD4 + T细胞的全身性自身免疫性疾病。在大鼠中,已证明自身反应性T细胞参与其中,而在小鼠中,注意力集中在“汞特异性”T细胞的证明上。为了阐明这些看似不同的T细胞参与情况,分析了用氯化汞处理1周或8周的B10.S小鼠的T细胞对各种含汞或不含汞的自身抗原(Ag)产生回忆反应的能力。短期用氯化汞处理的供体的T细胞未能对无汞抗原产生记忆反应,但对氯化汞产生了显著反应,并且还与含汞的自身抗原发生反应。有趣的是,长期用氯化汞处理的供体的T细胞表现出不同的反应模式。它们几乎不对氯化汞产生反应,对含汞的脾脏蛋白反应也很差,但对细胞核和原纤维蛋白有强烈反应,无论这些自身成分是否用氯化汞处理过。可以想象,识别与核自身蛋白(如原纤维蛋白)结合的汞的T细胞的初始激活最终导致对未改变的自身蛋白特异性的T细胞的激活。

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