Susceptibility of mice deficient in IL17 receptor to the development of Experimental Autoimmune prostatitis

BRESER ML, BERTOTTO ME, MACCIONI M, RIVERO VE

Congreso; FIRST FRENCH-ARGENTINE IMMUNOLOGY CONGRESS. FAIC 2010; 2010

Our laboratory has developed over the past decade a mouse model of experimental autoimmune prostatitis (EAP) that is considered a valid model for the human disease named Chronic prostatitis/chronic pelvic pain syndrome. In the present work we analyze the susceptibility of mice deficient in IL17 receptor IL17 (RIL17-/-) to the development of EAP. Prostate extract plus adjuvant was used to immunize wild type and RIL17-/- C57BL6 mice on days 0 and 15. Control groups immunized only with adjuvant were included. Mice were sacrificed at day 24 after immunization and the presence of antigen specific INFg, IL10 and IL17 producing cells was evaluated by ELISA and FACS. Infiltration of the prostate gland was also analyzed by conventional histology and FACS. No antigen specific INFg, IL10 and IL17 producing cells were observed in lymph nodes and spleen of control mice. Lower secretion of specific IL17 and INFg was observed in culture supernatants of RIL17-/- mice when compared with values observed in wild type mice (IL17= wt 893E}140 pg/ml, RIL17-/-: 178E}96 pg/ml; INFg= wt 2431E}348 pg/ml, RIL17-/-: 153E}140 pg/ ml). No significant differences were observed when specific IL10 was analyzed in both groups (IL10= wt 270E}70 pg/ml, RIL17-/-: 261E}43 pg/ml). When prostate sections were analyzed, mononuclear cell infiltration with epithelial acini atrophy was seen in C57BL6 wild type glands but neither infiltration nor lesions were observed in RIL17-/- mice. These results indicate that the absence of IL17R made mice resistant to EAP, being these mice not able to generate neither Th17 nor Th1cells. Our results argue for an important role of IL17R in EAP and suggest a cooperative relation between Th1 and Th17 cellsg, IL10 and IL17 producing cells was evaluated by ELISA and FACS. Infiltration of the prostate gland was also analyzed by conventional histology and FACS. No antigen specific INFg, IL10 and IL17 producing cells were observed in lymph nodes and spleen of control mice. Lower secretion of specific IL17 and INFg was observed in culture supernatants of RIL17-/- mice when compared with values observed in wild type mice (IL17= wt 893E}140 pg/ml, RIL17-/-: 178E}96 pg/ml; INFg= wt 2431E}348 pg/ml, RIL17-/-: 153E}140 pg/ ml). No significant differences were observed when specific IL10 was analyzed in both groups (IL10= wt 270E}70 pg/ml, RIL17-/-: 261E}43 pg/ml). When prostate sections were analyzed, mononuclear cell infiltration with epithelial acini atrophy was seen in C57BL6 wild type glands but neither infiltration nor lesions were observed in RIL17-/- mice. These results indicate that the absence of IL17R made mice resistant to EAP, being these mice not able to generate neither Th17 nor Th1cells. Our results argue for an important role of IL17R in EAP and suggest a cooperative relation between Th1 and Th17 cellsg, IL10 and IL17 producing cells were observed in lymph nodes and spleen of control mice. Lower secretion of specific IL17 and INFg was observed in culture supernatants of RIL17-/- mice when compared with values observed in wild type mice (IL17= wt 893E}140 pg/ml, RIL17-/-: 178E}96 pg/ml; INFg= wt 2431E}348 pg/ml, RIL17-/-: 153E}140 pg/ ml). No significant differences were observed when specific IL10 was analyzed in both groups (IL10= wt 270E}70 pg/ml, RIL17-/-: 261E}43 pg/ml). When prostate sections were analyzed, mononuclear cell infiltration with epithelial acini atrophy was seen in C57BL6 wild type glands but neither infiltration nor lesions were observed in RIL17-/- mice. These results indicate that the absence of IL17R made mice resistant to EAP, being these mice not able to generate neither Th17 nor Th1cells. Our results argue for an important role of IL17R in EAP and suggest a cooperative relation between Th1 and Th17 cellsg was observed in culture supernatants of RIL17-/- mice when compared with values observed in wild type mice (IL17= wt 893E}140 pg/ml, RIL17-/-: 178E}96 pg/ml; INFg= wt 2431E}348 pg/ml, RIL17-/-: 153E}140 pg/ ml). No significant differences were observed when specific IL10 was analyzed in both groups (IL10= wt 270E}70 pg/ml, RIL17-/-: 261E}43 pg/ml). When prostate sections were analyzed, mononuclear cell infiltration with epithelial acini atrophy was seen in C57BL6 wild type glands but neither infiltration nor lesions were observed in RIL17-/- mice. These results indicate that the absence of IL17R made mice resistant to EAP, being these mice not able to generate neither Th17 nor Th1cells. Our results argue for an important role of IL17R in EAP and suggest a cooperative relation between Th1 and Th17 cellsg= wt 2431E}348 pg/ml, RIL17-/-: 153E}140 pg/ ml). No significant differences were observed when specific IL10 was analyzed in both groups (IL10= wt 270E}70 pg/ml, RIL17-/-: 261E}43 pg/ml). When prostate sections were analyzed, mononuclear cell infiltration with epithelial acini atrophy was seen in C57BL6 wild type glands but neither infiltration nor lesions were observed in RIL17-/- mice. These results indicate that the absence of IL17R made mice resistant to EAP, being these mice not able to generate neither Th17 nor Th1cells. Our results argue for an important role of IL17R in EAP and suggest a cooperative relation between Th1 and Th17 cells