• Experimental autoimmune encephalomyelitis treatment;
  • Tcell anergy;
  • Peptides;
  • Multiple sclerosis


In susceptible strains of mice, myelin basic protein (MBP) peptide Ac1-11 induces experimental autoimmune encephalomyelitis (EAE) providing a useful model for human multiple sclerosis. Ac1-11 binds major histocompatibility complex (MHC) class II molecules Aαuu. Here, we show that the Ac1-11 peptide, when administered intraperitoneally in incomplete Freund's adjuvant (IFA) emulsion, can effectively treat Ac1-11-induced EAE in mice. Treatment with Ac1-11/IFA 9 days after initial immunization with Ac1-11 in complete Freund's adjuvant (CFA) results in a loss of T cell proliferation to MBP Ac1-11. This lack of T cell proliferation is not due to T cell anergy and is not specific. A similar lack of T cell proliferation and inhibition of EAE is observed when an ovalbumin peptide OVA323–339 or a sperm whale myoglobin peptide SWM110-121 are used to treat mice immunized with Ac1-11. Interestingly, we show that previously unresponsive lymph node cells from treated mice respond normally if Ac1-11 is presented by fresh antigen-presenting cells taken from normal mice. These results argue that the lack of T cell proliferation and inhibition of EAE is not due to specific T cell anergy as suggested by others. Instead this appears to be due to blocking of MHC class II molecules Aαuu by the treating peptides.