Moudgil Kamal D, Durai Malarvizhi
Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Trends Immunol. 2008 Sep;29(9):412-8. doi: 10.1016/j.it.2008.06.003.
Heat-shock proteins (hsps) are highly conserved and immunogenic, and they are generally perceived to be attractive initiators or targets of a pathogenic immune response, and as such, have been implicated in the pathogenesis of autoimmune arthritis. However, studies in animal models and arthritis patients have unraveled the disease-regulating attributes of self-hsp65. We propose that the self-hsp65 induces a protective and beneficial immune response because of its ubiquitous distribution, stress inducibility and participation in tolerogenic processes. By contrast, the foreign hsp65 that does not influence the above processes and that resides admixed with microbial ligands for innate receptors generates an inflammatory pathogenic response. The regulatory properties of self-hsps need be fully explored and might be used for therapeutic purposes.
热休克蛋白（hsps）具有高度保守性和免疫原性，通常被认为是致病性免疫反应的诱人引发剂或靶点，因此与自身免疫性关节炎的发病机制有关。然而，对动物模型和关节炎患者的研究揭示了自身hsp65的疾病调节特性。我们认为，自身hsp65因其广泛分布、应激诱导性以及参与耐受性过程而诱导产生保护性和有益的免疫反应。相比之下，不影响上述过程且与天然受体的微生物配体混合存在的外来hsp65会引发炎症性致病反应。自身热休克蛋白的调节特性有待充分探索，可能用于治疗目的。
