Different murine models of autoimmune
prostatitis have been developed and characterized, proving the autoimmune origin of this pathology. Autoimmune
prostatitis models have also provided a wealth of information on the mechanisms involved in disease development, shedding light on inciting
autoantigens, regulatory and pathogenic T cells, and mediators of prostatic autoimmunity. Unfortunately, the clinical counterparts of experimental autoimmune
prostatitis are still poorly defined. In this review, we will discuss evidence for the autoimmune origin of chronic
prostatitis/chronic
pelvic pain syndrome (CP/CPPS) and the chronic inflammatory nature of
benign prostatic hyperplasia (BPH). The autoimmune pathogenesis of CP/CPPS and the chronic
inflammation characteristic of BPH will be reviewed within the context of the recent demonstration that human prostate stromal cells from BPH tissue can act as antigen-presenting cells and are not only able to activate CD4(+) T lymphocytes, but can also produce
IL-12 and
IL-23, which are key
cytokines for the induction of pathogenic Th1 and Th17 cells.