van Eden W, Hogervorst E J, van der Zee R, van Embden J D, Hensen E J, Cohen I R
Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, University of Utrecht, The Netherlands.
Rheumatol Int. 1989;9(3-5):187-91. doi: 10.1007/BF00271878.
Arthritis - induced experimentally in rats by immunization with mycobacteria has been shown to depend on specific T cell recognition of an epitope present on the mycobacterial 65-kD heat-shock protein. This particular epitope has been observed to have a structural mimicry with a cartilage-associated molecule present in the joints. Since the bacterial heat-shock proteins and the cartilage-associated molecules are of a conserved nature, one might infer from the experimental model that in humans similar mimicry could play a role in the initiation of autoimmune arthritis. Recent findings from the analysis of immunological reactivity to the 65-kD in rheumatoid arthritis patients seem to support such a role for the mycobacterial 65-kD heat-shock protein in human disease.
通过用分枝杆菌免疫在大鼠中实验性诱导的关节炎已被证明取决于对分枝杆菌65-kD热休克蛋白上存在的一个表位的特异性T细胞识别。已观察到这个特定表位与关节中存在的一种软骨相关分子具有结构模拟性。由于细菌热休克蛋白和软骨相关分子具有保守性质,从该实验模型可以推断,在人类中类似的模拟可能在自身免疫性关节炎的起始中起作用。类风湿性关节炎患者对65-kD的免疫反应性分析的最新发现似乎支持分枝杆菌65-kD热休克蛋白在人类疾病中的这种作用。