Gaston J S
Department of Rheumatology, University of Birmingham, UK.
Int J Clin Lab Res. 1992;22(2):90-4. doi: 10.1007/BF02591403.
Heat shock proteins (HSPs) have been postulated to be critical antigens in both autoimmune disease and experimental models of autoimmunity. This postulate has been largely based on the remarkable conservation of aminoacid sequence between human and bacterial HSPs, so that it has been argued that immune responses initially directed against the HSP of an infectious agent, would have the potential to initiate or maintain autoimmune disease. This would apply especially to T cell recognition of HSPs, since the T cell focuses on short peptide epitopes within a protein antigen rather than on the antigen's secondary structure. This article critically evaluates the available experimental evidence relating to this hypothesis: although research has clearly highlighted the central role of HSPs in the cellular immune response to pathogenic organisms and has shown the potential for T cell responses directed against self HSPs, a role for self HSPs as major target antigens in autoimmune disease has yet to be firmly established.
热休克蛋白（HSPs）被认为是自身免疫性疾病和自身免疫实验模型中的关键抗原。这一假设主要基于人类和细菌热休克蛋白之间氨基酸序列的显著保守性，因此有人认为，最初针对感染因子热休克蛋白的免疫反应有可能引发或维持自身免疫性疾病。这尤其适用于热休克蛋白的T细胞识别，因为T细胞关注的是蛋白质抗原内的短肽表位，而不是抗原的二级结构。本文批判性地评估了与该假设相关的现有实验证据：尽管研究清楚地突出了热休克蛋白在针对致病生物体的细胞免疫反应中的核心作用，并显示了针对自身热休克蛋白的T细胞反应的可能性，但自身热休克蛋白作为自身免疫性疾病主要靶抗原的作用尚未得到确凿证实。
