The Hypermethylation Of Foxp3 Promoter Impairs The Function Of Treg Cells In EAP

Objective Treg cells are crucial for maintaining immune homeostasis in CP/CPPS,but the molecular mechanisms underlying the modulation of the function of Treg in CP/CPPS remain unclear.Methods EAP model was induced by subcutaneous injecting prostate-steroid-binding protein(PBSP)and complete Freund's adjuvant with NOD mice.Histological analysis of the prostate,expression of IFN-?,TGF-? and IL-10 in serum,suppressive function of Tregs on Teffs,percentage of Tregs in splenic lymphocyte,methylation status of Foxp3 promoter,expression of Foxp3 were performed and measured.Subsequently,we examined the effects of DNA-methylation inhibitor 5-aza-2-deoxycytidine(Aza)in EAP model mice.Results Histological analysis revealed that EAP model was successfully induce with PBSP.The expression of IFN-?was increased,and TGF-?was decreased in serum of EAP,respectively.The suppressive ability of Tregs on Teffs was impaired in EAP.The percentage of Tregs in splenic lymphocyte was increased in EAP.The methylation level of Foxp3 promoter was increased and the expression of Foxp3 was decreased in EAP.Prostate inflammation was alleviated with methylation inhibitor AZA in EAP mice,and expression of TGF-? and Foxp3 were increased,suppressive function of Tregs was improved.Conclusions The results suggest that aberrant increased methylation of Foxp3 promoter in Treg cells impair the suppressive function of Treg cells,exacerbating autoimmune inflammatory injury in EAP.