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.
