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

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.

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

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

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