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 (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 INFy, 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 INFy, IL10 and IL17 producing cells were observed in lymph nodes and spleen of control mice. Lower secretion of specific IL17 and INFy was observed in culture supernatants of RIL17-/- mice when compared with values observed in wild type mice (IL17= wt 893„b140 pg/ml, RIL17-/-: 178„b96 pg/ml; INFy= wt 2431¡Ó348 pg/ml, RIL17-/-: 153¡Ó140 pg/ml). No significant differences were observed when specific IL10 was analyzed in both groups (IL10= wt 270„b70 pg/ml, RIL17-/-: 261„b43 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. |