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氯化汞诱导的棕色挪威大鼠自身抗体的动力学和致病性

Kinetics and pathogenicity of autoantibodies induced by mercuric chloride in the brown Norway rat.

作者信息

Pusey C D, Bowman C, Morgan A, Weetman A P, Hartley B, Lockwood C M

机构信息

Department of Medicine, Royal Postgraduate Medical School, London, England.

出版信息

Clin Exp Immunol. 1990 Jul;81(1):76-82. doi: 10.1111/j.1365-2249.1990.tb05294.x.

DOI:10.1111/j.1365-2249.1990.tb05294.x
PMID:2199099
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1535003/
Abstract

Repeated low-dose injections of mercuric chloride (HgCl2) in the brown Norway (BN) rat result in polyclonal activation which includes the induction of anti-glomerular basement membrane (GBM) autoantibodies. We examined the kinetics of various autoantibodies produced in vivo, general features of polyclonal activation such as total IgG levels and immune complex formation, and the relationship between organ specific autoimmunity and tissue injury in the kidney and thyroid. The production of immune complexes and autoantibodies to GBM and thyroglobulin was short lived, and the increase in levels of total IgG and antibodies to ssDNA and dsDNA was prolonged; the antibody response to collagen types I and II was intermediate in duration. Autoantibodies induced by HgCl2 caused only mild and variable tissue injury in the kidneys and did not induce abnormalities in the thyroid. These studies demonstrate that immunostimulation by mercury may result in the formation of a range of autoantibodies, with variable kinetics and pathogenicity.

摘要

在棕色挪威(BN)大鼠中反复低剂量注射氯化汞(HgCl2)会导致多克隆激活,其中包括诱导抗肾小球基底膜(GBM)自身抗体。我们研究了体内产生的各种自身抗体的动力学、多克隆激活的一般特征,如总IgG水平和免疫复合物形成,以及肾脏和甲状腺中器官特异性自身免疫与组织损伤之间的关系。免疫复合物以及针对GBM和甲状腺球蛋白的自身抗体的产生是短暂的,而总IgG以及针对单链DNA和双链DNA的抗体水平的升高则持续时间较长;对I型和II型胶原的抗体反应持续时间处于中间水平。HgCl2诱导的自身抗体仅在肾脏中引起轻度且多变的组织损伤,并未在甲状腺中诱发异常。这些研究表明,汞引起的免疫刺激可能导致一系列自身抗体的形成,其动力学和致病性各不相同。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ef8/1535003/4a321240ef8c/clinexpimmunol00070-0082-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ef8/1535003/4a321240ef8c/clinexpimmunol00070-0082-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ef8/1535003/4a321240ef8c/clinexpimmunol00070-0082-a.jpg

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本文引用的文献

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Collagen-induced arthritis in the rat: modification of immune and arthritic responses by free collagen and immune anti-collagen antiserum.大鼠胶原诱导性关节炎:游离胶原和免疫抗胶原抗血清对免疫和关节炎反应的影响
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在使用利巴韦林和α干扰素进行抗丙型肝炎病毒治疗期间,人类自身抗体对细胞质杆状和环状结构反应的时间演变。
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A role for alphabeta T cells in the resistant phase of the Brown Norway rat model of vasculitis.αβ T细胞在棕色挪威大鼠血管炎模型抵抗期的作用。
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Resistance to re-challenge in the Brown Norway rat model of vasculitis is not always complete and may reveal separate effector and regulatory populations.在褐家鼠血管炎模型中,再次激发时的抵抗并不总是完全的,可能会揭示出不同的效应细胞群和调节细胞群。
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