Autoantigen specific IL-2 activated CD4+CD25+T regulatory cells inhibit induction of experimental autoimmune neuritis

Experimental autoimmune neuritis (EAN) induced by peripheral nerve myelin (PNM) is self-limiting and re-immunization with PNM does not re-activate disease. This study showed inhibition of EAN by CD4+CD25+T cells both from sensitized hosts or from naïve hosts after ex-vivo activation by PNM and rIL-2. Transfer of naïve CD4+CD25+T cells has no effect on EAN, nor did naïve CD4+CD25+T cells activated with rIL-2 and renal tubular antigen. Culture of naive CD4+CD25+Treg with rIL-2 and PNM induced mRNA for the IFN-gamma receptor. We showed naïve CD4+CD25+T cells activated by specific auto-antigen and rIL-2 produced more potent antigen-specific Treg that may have therapeutic potential. •CD4+CD25+Treg from animals after recovery from EAN transfer protection from EAN in naïve hosts•Naïve CD4+CD25+Treg activated by specific antigen (PNM) and rIL-2 transfer protection from EAN.•Naïve CD4+CD25+Treg activated by a third-party autoantigen and rIL-2 do not protect against EAN.•Naïve CD4+CD25+Treg activated by antigen and rIL-2, express mRNA for IFNGR, and are Ts1 cells.•Ex Vivo activated antigen-specific Treg may be of therapeutic use in treatment of autoimmunity.