Prostatein or steroid binding protein (PSBP) induces experimental autoimmune prostatitis (EAP) in NOD mice.
In a previous study, we showed that nonobese diabetic (NOD) mice, a strain that present an inherited predisposition to develop both spontaneous and induced autoimmune lesions, are susceptible to the induction of experimental autoimmune prostatitis (EAP), developing a severe inflammatory reaction in the prostate, accompanied by humoral and T-cell-mediated responses. In this study we asked whether the protein steroid binding protein (PSBP) or prostatein (a major autoantigen in the rat model of EAP) is a potential autoantigen in the NOD mouse model and examined the ability of purified PSBP to induce EAP in this strain. Our results indicate clearly that NOD male mice react immunologically to PSBP by developing lymphocytic inflammatory lesions in prostatic tissue and producing both a cellular- and humoral-specific autoimmune response. But our results suggest also the existence of other prostatic autoantigens present only in total prostate extract. Such additional antigens could enhance the autoimmune response and result in more severe forms of inflammation. We also analyzed the respective contributions of MHC antigens and CD4/CD8 T-cell subsets in NOD mice lacking expression of beta 2-microglobulin (NOD.beta2m degrees/degrees) or MHC class II beta chain (NOD.Abeta degrees/degrees) and demonstrate an essential role for CD4(+) T cells in the development of EAP in the NOD model. In conclusion, we demonstrate that PSBP is an autoantigen recognized by the NOD immune system, capable of generating humoral and cellular autoimmune responses and of inducing EAP. Moreover, using selected knock-out NOD mice we demonstrate an essential role for CD4(+) T cells in the development of EAP.
Rivero
Virginia
V
Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina. vrivero@bioclin.fcq.unc.edu.ar
Carnaud
Claude
C
Riera
Clelia Maria
CM
D000727:Androgen-Binding Protein / Q000276:immunology*; D000818:Animals; D001323:Autoantibodies / Q000097:blood; D001324:Autoantigens; D001327:Autoimmune Diseases / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000235:genetics; D007114:Immunization; D066298:In Vitro Techniques; D007700:Kinetics; D008213:Lymphocyte Activation; D008297:Male; D051379:Mice; D016688:Mice, Inbred NOD; D018345:Mice, Knockout; D060789:Prostatein; D011472:Prostatitis / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D060765:Secretoglobins; D014598:Uteroglobin; D001613:beta 2-Microglobulin / Q000172:deficiency / Q000235:genetics; D060788:Mammaglobin B
D000727:Androgen-Binding Protein; D001323:Autoantibodies; D001324:Autoantigens; D000949:Histocompatibility Antigens Class II; D060789:Prostatein; D060765:Secretoglobins; D014598:Uteroglobin; D001613:beta 2-Microglobulin; C511484:Scgb1d2 protein, rat; C511483:Scgb1d4 protein, rat; C556468:Scgb2a1 protein, rat; D060788:Mammaglobin B