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 IL-17 receptor (RIL17) to the development of EAP. Prostate extract plus adjuvant was used to immunize C5-BL/6 wild type and C57BL/6-RIL17-/- 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 INF-ã, IL-10 and IL-17 producing cells was evaluated by ELISA and FACS. Infiltration of the prostate gland was also analyzed by conventional histology and FACS.
No antigen specific INF-ã, IL-10 and IL-17 producing cells were observed in lymph nodes and spleen of control mice. Lower secretion of specific IL-17 and INFã was observed in culture supernatants of C57BL/6-RIL17-/- mice when compared with values observed in C57BL6 mice. No significant differences were observed when specific IL-10 was analyzed in both groups. When prostate sections were analyzed, mononuclear cell infiltration with epithelial acine atrophy was seen in C57BL6 wild type glands but neither infiltration nor lesions were observed in C57BL6-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 Th1 cells. Our results argue for an important role of IL17R in EAP and suggest a cooperative relation between Th1 and Th17 cells.
