Findings in CP/CPPS patients |
Specific T cell responses and IFNγ secretion to prostate antigens (PAg) and seminal proteins |
(39–44) |
Serum PAg-specific IgG |
(45) |
Prostate tissue Ig deposition, prostate leukocyte, and T cell infiltration |
(46–48) |
Increased numbers of leukocytes (granulocytes, macrophages, T, and B cells) in expressed prostate secretions (EPS), urine after prostatic massage, or semen |
(16, 29, 49–51) |
Increased levels of immunoglobulins, inflammatory cytokines, chemokines, and mast cell mediators in EPS or seminal plasma |
(16, 47, 50, 52–60) |
Findings in animal models of autoimmune prostatitis |
Macrophages, DCs, mast cells, CD4+ and CD8+ T and B cells infiltrating the prostate |
(61–72, 79–91) |
CD4+ T cells are essential in driving prostatitis |
(63) |
Th1/Th17-associated autoimmune responses to PAg |
(64–66, 83, 91) |
PAg-specific immune response is associated to a Th1 cytokine and immunoglobulin isotype pattern |
(83, 84) |
Crucial role of IFNg in mediating pathology |
(62, 65–67) |
CXCR3 and CCR5 expressing PAg-specific Th1 cells mediate disease induction |
(66) |
IL-17 is dispensable for disease and pain development |
(67) |
Treg function condition disease and pain induction |
(68) |
Pelvic pain development correlated with inflammation |
(67, 69) |
Increased tryptase-B and nerve growth factor (NGF) in prostate tissue |
(70) |
Mast cells mediate pelvic pain development |
(71) |
CCL2, CCL3, and tryptase-B involved in pain development |
(72) |
Increased NGF and neuronal density in prostate tissue |
(73) |