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D-青霉胺诱导的棕色挪威大鼠自身免疫。与氯化汞诱导的自身免疫的相似性。

D-penicillamine-induced autoimmunity in Brown-Norway rats. Similarities with HgCl2-induced autoimmunity.

作者信息

Tournade H, Pelletier L, Pasquier R, Vial M C, Mandet C, Druet P

机构信息

From INSERM U 28, Hôpital Broussais, Paris, France.

出版信息

J Immunol. 1990 Apr 15;144(8):2985-91.

PMID:2139074
Abstract

D-penicillamine (DP) has been previously shown to induce an autoimmune disease in Brown-Norway (BN) rats, characterized by a dermatitis, by the production of antinuclear antibodies, by the formation fo circulating immune complexes, and by linear IgG deposits along the glomerular basement membrane. These manifestations are quite similar to those observed in mercuric chloride (HgCl2)-induced autoimmunity. The mechanism of the latter disease has been recently partly elucidated. The aim of this study was to compare DP and HgCl2-induced autoimmunity in BN rats and to compare the mechanisms involved in both situations. A transient increase in the number of spleen cells, affecting B cells and CD4+ T cells, and an increase in serum IgE concentration, previously reported in HgCl2-induced autoimmunity, were observed during DP treatment. Autoreactive anti-class II T cells able to proliferate not only in the presence of autologous B cells but also in the presence of syngeneic normal B cells were found in DP-treated BN rats. Spontaneous regulation occurred, associated with the disappearance of autoreactive T cells. Suppressor CD8+ T cells were not involved in this phenomenon. Mechanisms involved in both the induction and the regulation of DP-induced autoimmunity seem to be quite similar to those reported in HgCl2-induced autoimmunity.

摘要

先前已表明,D-青霉胺(DP)可在棕色挪威(BN)大鼠中诱发自身免疫性疾病,其特征为皮炎、产生抗核抗体、形成循环免疫复合物以及沿肾小球基底膜出现线性IgG沉积。这些表现与氯化汞(HgCl2)诱发的自身免疫中观察到的表现非常相似。后一种疾病的机制最近已部分阐明。本研究的目的是比较DP和HgCl2在BN大鼠中诱发的自身免疫,并比较两种情况下涉及的机制。在DP治疗期间,观察到先前在HgCl2诱发的自身免疫中报道的脾细胞数量短暂增加,影响B细胞和CD4+T细胞,以及血清IgE浓度升高。在经DP处理的BN大鼠中发现了自身反应性抗II类T细胞,其不仅能在自体B细胞存在时增殖,还能在同基因正常B细胞存在时增殖。发生了自发调节,与自身反应性T细胞的消失有关。抑制性CD8+T细胞不参与这一现象。DP诱发的自身免疫的诱导和调节所涉及的机制似乎与HgCl2诱发的自身免疫中报道的机制非常相似。

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