title: Stress proteins as inducers and targets of regulatory T cells in arthritis.
abstract: Immunization with microbial or mammalian stress proteins or heat-shock proteins in models of experimental autoimmunity has been observed to lead to increased disease resistance. Furthermore, such immunization has been proposed to result in the induction and expansion of T cells that suppress disease upon transfer. Comparisons of microbial heat-shock proteins with other conserved immunogenic proteins of bacterial origin have indicated a unique capacity for heat-shock proteins to induce a regulatory phenotype in T cells, such as reflected by the production of IL10. Also, studies in children with chronic arthritis have indicated that T-cell responses to heat-shock proteins are associated with a benign course of the disease and with remission. Furthermore, in patients, heat-shock-protein-(HSP-) activated T cells were shown to display regulatory phenotypes consistent with CD4+ CD25+ T regulatory cells.
authors.affiliation: Division of Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.
authors.forename: Willem
authors.initials: W
authors.lastname: van Eden
authors.forename: Femke
authors.initials: F
authors.lastname: Hauet-Broere
authors.forename: Suzanne
authors.initials: S
authors.lastname: Berlo
authors.forename: Liesbeth
authors.initials: L
authors.lastname: Paul
authors.forename: Ruurd
authors.initials: R
authors.lastname: van der Zee
authors.forename: Isme
authors.initials: I
authors.lastname: de Kleer
authors.forename: Berent
authors.initials: B
authors.lastname: Prakken
authors.forename: Leonie
authors.initials: L
authors.lastname: Taams
mesh_terms: D000818:Animals; D001169:Arthritis, Experimental / Q000276:immunology*; D006360:Heat-Shock Proteins / Q000502:physiology*; D016753:Interleukin-10 / Q000096:biosynthesis; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism
chemical_list: D006360:Heat-Shock Proteins; D016753:Interleukin-10