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人类免疫缺陷病毒1型(HIV-1)与抗原受体分子之间的分子模拟:艾滋病发病机制的线索

Molecular mimicry between HIV-1 and antigen receptor molecules: a clue to the pathogenesis of AIDS.

作者信息

Süsal C, Kröpelin M, Daniel V, Opelz G

机构信息

Department of Transplantation Immunology, Institute of Immunology, University of Heidelberg, FRG.

出版信息

Vox Sang. 1993;65(1):10-7. doi: 10.1111/j.1423-0410.1993.tb04518.x.

Abstract

There is increasing evidence that autoimmune phenomena play an important role in the immunopathogenesis of AIDS. We found a high degree of sequence homology between HIV-1 and antigen receptor molecules, immunoglobulins and T cell receptors. Based on recent findings that the appearance of anti-Fab autoantibodies and attachment of gp120/immunoglobulin/complement complexes on CD4+ T cells are associated with the decrease of CD4+ T cells in HIV-infected patients, we hypothesize herein that cross-reactive anti-F (ab')2 autoantibodies and circulating gp120 molecules are responsible for a destabilization of the immune network and the elimination of CD4+ T cells.

摘要

越来越多的证据表明,自身免疫现象在艾滋病的免疫发病机制中起重要作用。我们发现HIV-1与抗原受体分子、免疫球蛋白和T细胞受体之间存在高度的序列同源性。基于最近的研究发现,抗Fab自身抗体的出现以及gp120/免疫球蛋白/补体复合物在CD4+ T细胞上的附着与HIV感染患者CD4+ T细胞的减少有关,我们在此假设,交叉反应性抗F(ab')2自身抗体和循环中的gp120分子导致免疫网络不稳定并致使CD4+ T细胞被清除。

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