IL-10 is critically involved in mycobacterial HSP70 induced suppression of proteoglycan-induced arthritis

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Background: The anti-inflammatory capacity of heat shock proteins (HSP) has been demonstrated in various animal models of inflammatory diseases and in patients. However, the mechanisms underlying this anti-inflammatory capacity are poorly understood. Therefore, the possible protective potential of HSP70 and its mechanisms were studied in proteoglycan (PG) induced arthritis (PGIA), a chronic and relapsing, T cell mediated murine model of arthritis. Methodology/Principal Findings: HSP70 immunization, 10 days prior to disease induction with PG, inhibited arthritis both clinically and histologically. In addition, it significantly reduced PG-specific IgG2a but not IgG1 antibody production. Furthermore, IFN-γ and IL-10 production upon in vitro restimulation with HSP70 was indicative of the induction of an HSP70-specific T cell response in HSP70 immunized mice. Remarkably, HSP70 treatment also modulated the PG-specific T cell response, as shown by the increased production of IL-10 and IFN-γ upon in vitro PG restimulation. Moreover, it increased IL-10 mRNA expression in CD4+CD25+cells. HSP70 vaccination did not suppress arthritis in IL-10-/-mice, indicating the crucial role of IL-10 in the protective effect. Conclusions/Significance: In conclusion, a single mycobacterial HSP70 immunization can suppress inflammation and tissue damage in PGIA and results in an enhanced regulatory response as shown by the antigen-specific IL-10 production. Moreover, HSP70 induced protection is critically IL-10 dependent. © 2009 Wieten et al.




Wieten, L., Berlo, S. E., ten Brink, C. B., van Kooten, P. J., Singh, M., van der Zee, R., … Broere, F. (2009). IL-10 is critically involved in mycobacterial HSP70 induced suppression of proteoglycan-induced arthritis. PLoS ONE, 4(1).

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