Analysis of the immune response and the prostate-reactive T cell repertoire in a mouse model of Experimental Autoimmune Prostatitis in NOD mice

MOTRICH RD; BRESER ML; RIVERO VE

Milan

Congreso; 15th International Congress of Immunology; 2013

International Union of Immunology Societies

Autoimmunity has been proposed as an etiology of the prevalent disease Chronic Pelvic Pain Syndrome. Experimental Autoimmune Prostatitis (EAP) model has proved useful for the study of CPPS because it has mirrored most findings in patients. Herein, we studied the immune response and the prostate-reactive T cell repertoire in EAP in NOD mice. Six- to 8-week-old NOD/LtJ mice were immunized with a prostate protein extract (PAg group), purified Prostatein (PSBP group), or vehicle (Control group) at days 0 and 15. Animals were euthanized on days 10 and 24 and the specific immune response was evaluated. CDR3-lenght spectratyping analysis of the prostate-reactive T cell repertoire from spleen, prostate-infiltrating cells and from a PSBP-specific short term cell line was performed. T-cell-mediated response showed a specific response characterized by enhanced proliferation and high levels of IFN-gamma, IL-2 and IL-17 secretion that could be detected in spleen and draining LN cells of mice from groups PAg and PSBP. Conversely, low-to-null levels of IL-4 were detected. Prostate infiltration and tissue damage accompanied that response. Also, high levels of IFN-gamma secretion were observed in a PSBP-specific cell line from autoimmune animals that transferred disease to naïve recipients. Clonotypes bearing TCR VB5.1, VB7, VB10 and VB15 were detected in spleen and prostate infiltrating cells from diseased animals and also in the PSBP-specific cell line. A strong Th1 response and the public clonotypes VB5.1, VB7, VB10 and VB15 are induced after immunization in EAP. These clonotypes secrete high levels of IFN-gamma and infiltrate the target organ causing disease.