title: Stress, heat shock proteins, and autoimmunity: how immune responses to heat shock proteins are to be used for the control of chronic inflammatory diseases.
abstract: Especially since the (re-)discovery of T cell subpopulations with specialized regulatory activities, mechanisms of anti-inflammatory T cell regulation are studied very actively and are expected to lead to the development of novel immunotherapeutic approaches, especially in chronic inflammatory diseases. Heat shock proteins (Hsp) are possible targets for regulatory T cells due to their enhanced expression in inflamed (stressed) tissues and the evidence that Hsp induce anti-inflammatory immunoregulatory T cell responses. Initial evidence for an immunoregulatory role of Hsp in chronic inflammation was obtained through analysis of T cell responses in the rat model of adjuvant arthritis and the findings that Hsp immunizations protected against the induction of various forms of autoimmune arthritis in rat and mouse models. Since then, immune reactivity to Hsp was found to result from inflammation in various disease models and human inflammatory conditions, such as rheumatoid arthritis (RA), type 1 diabetes, and atherosclerosis. Now, also in the light of a growing interest in T cell regulation, it is of interest to further explore the mechanisms through which Hsp can be utilized to trigger immunoregulatory pathways, capable of suppressing such a wide and diversified spectrum of inflammatory diseases.
authors.affiliation: Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Yalelaan 1, Utrecht University, 3584CL Utrecht, the Netherlands. w.vaneden@uu.nl
authors.forename: Willem
authors.initials: W
authors.lastname: Van Eden
authors.forename: George
authors.initials: G
authors.lastname: Wick
authors.forename: Salvatore
authors.initials: S
authors.lastname: Albani
authors.forename: Irun
authors.initials: I
authors.lastname: Cohen
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000378:metabolism* / Q000473:pathology* / Q000628:therapy; D002908:Chronic Disease; D006360:Heat-Shock Proteins / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism* / Q000628:therapy*; D018384:Oxidative Stress / Q000276:immunology*
chemical_list: D006360:Heat-Shock Proteins