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Stress, Heat Shock Proteins, and Autoimmunity
Author(s) -
VAN EDEN WILLEM,
WICK GEORGE,
ALBANI SALVATORE,
COHEN IRUN
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1391.020
Subject(s) - autoimmunity , heat shock protein , inflammation , immunology , arthritis , rheumatoid arthritis , immune system , t cell , autoimmune disease , biology , cell , regulatory t cell , medicine , antibody , il 2 receptor , genetics , gene
: 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.