Stress proteins as inducers and targets of regulatory T cells in arthritis.
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.
van Eden
Willem
W
Division of Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.
Hauet-Broere
Femke
F
Berlo
Suzanne
S
Paul
Liesbeth
L
van der Zee
Ruurd
R
de Kleer
Isme
I
Prakken
Berent
B
Taams
Leonie
L
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
D006360:Heat-Shock Proteins; D016753:Interleukin-10