van der Zee R, Anderton S M, Prakken A B, Liesbeth Paul A G, van Eden W
Department of Immunology, Faculty of Veterinary Medicine, University of Utrecht, The Netherlands.
Semin Immunol. 1998 Feb;10(1):35-41. doi: 10.1006/smim.1997.0103.
The relationships between bacterial heat shock proteins (HSPs) and autoimmunity were first disclosed in the mycobacteria-induced model of adjuvant arthritis: passive transfer of a T cell clone responding to mycobacterial HSP60 evoked disease in naive recipient animals. However, the disease could not be induced by immunization with HSP60, but instead protection was established. Subsequently, similar protection was found in experimental models of arthritis that do not involve challenge with bacterial antigens for the induction of disease. This rather general protective potency of bacterial HSPs against arthritis seems to result from the capacity of strongly conserved sequences in the protein to activate T cells that cross-recognize the mammalian homologous HSP-sequences presented on cells at the site of inflammation. It is possible that immunological recognition of bacterial HSPs is part of a general strategy used by the immune system for the regulatory control of the potentially harmful recognition of autoantigens as a hedge against the development of autoimmune disease.
细菌热休克蛋白（HSPs）与自身免疫之间的关系最初是在分枝杆菌诱导的佐剂性关节炎模型中被揭示的：对分枝杆菌HSP60有反应的T细胞克隆的被动转移在未接触过抗原的受体动物中引发了疾病。然而，用HSP60免疫并不能诱导疾病，反而建立了保护作用。随后，在不涉及用细菌抗原激发来诱导疾病的关节炎实验模型中也发现了类似的保护作用。细菌HSPs对关节炎的这种相当普遍的保护效力似乎源于该蛋白中高度保守序列激活T细胞的能力，这些T细胞能交叉识别炎症部位细胞上呈现的哺乳动物同源HSP序列。细菌HSPs的免疫识别可能是免疫系统用于对自身抗原潜在有害识别进行调节控制的一般策略的一部分，以此作为预防自身免疫性疾病发生的一种保护措施。
