MOTRICH RUBEN DARIO
Congresos y reuniones científicas
Título:
Experimental Autoimmune Prostatitis: the role of IFN-gamma
Autor/es:
RUBEN MOTRICH; EVELYNE VAN ETTEN; CLELIA RIERA; CHANTAL MATHIEU; VIRGINIA RIVERO
Lugar:
Rio de Janeiro, Brasil
Reunión:
Congreso; 13th Internacional Congreso of Immunology.; 2007
Institución organizadora:
International Union of Immunology Societies
Resumen:
Autoimmune prostatitis has been proposed as a cause of Chronic-Pelvic-Pain-Syndrome. Autoimmunity against prostate antigens of a Th1-associated pattern was evidenced in humans and animal models. This work aimed to establish the role of IFN-gamma in Experimental Autoimmune Prostatitis (EAP), by studying mice defficient in crucial transcription factors in the IFN-gamma-signalling cascade: IRF-1 and STAT-1. EAP development was analyzed in C57BL/6, IRF1-KO and STAT1-KO mice as well as in the autoimmune prone NOD mouse model. EAP was induced by the immunization with Prostatein (PSBP) in CFA, while control mice received saline solution plus CFA. PSBPimmunized NOD mice evidenced severe infiltration and lessions in prostatic tissue. In parallel, prostate RT- PCR analysis revealed a significant increase in IFN-gamma and IL-12 levels, and a decrease in IL-10 levels. A strong PSBPspecific
cellular and humoral autoimmune response, with high IFN-gamma secretion and IgG2a autoantibodies, were revealed. In contrast, reduced PSBP-specific T cell lymphoproliferation with decreased IFN-gamma secretion was detected in autoimmune IRF1-KO and STAT1-KO mice when compared to C57BL/6 wild-type mice. The humoral autoimmune response was characterized by high titers of IgG1 and no specific IgG2a. Finally, PSBP-immunized IRF1-KO and STAT1-KO mice evidenced absent to mild inflammation in prostatic tissue, demonstrating that the autoimmune response developed by these animals was incapable of inducing the typical prostatic lessions of the EAP. In conclusion, these findings support a key role of IFN-gamma in the pathogenesis of EAP.
cellular and humoral autoimmune response, with high IFN-gamma secretion and IgG2a autoantibodies, were revealed. In contrast, reduced PSBP-specific T cell lymphoproliferation with decreased IFN-gamma secretion was detected in autoimmune IRF1-KO and STAT1-KO mice when compared to C57BL/6 wild-type mice. The humoral autoimmune response was characterized by high titers of IgG1 and no specific IgG2a. Finally, PSBP-immunized IRF1-KO and STAT1-KO mice evidenced absent to mild inflammation in prostatic tissue, demonstrating that the autoimmune response developed by these animals was incapable of inducing the typical prostatic lessions of the EAP. In conclusion, these findings support a key role of IFN-gamma in the pathogenesis of EAP.
