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A Viral Peptide with Limited Homology to a Self Peptide Can Induce Clinical Signs of Experimental Autoimmune Encephalomyelitis¹

Anand M. Gautam^2,*, Roland Liblau, Gareth Chelvanayagam, Lawrence Steinman^§ and Tanya Boston^*

^* Antigen Presentation Laboratory, Division of Immunology and Cell Biology and Human Genetics Group, Division of Molecular Medicine, John Curtin School of Medical Research, Australian National University, Canberra, Australia; and Cellular Immunology Laboratory and ^§ Institut National de la Santé et de la Recherche Médicale, CJF 9608, Pitie-Salpetriere Hospital, Paris, France

Molecular mimicry has been suggested as a mode of autoreactive T cell stimulation in autoimmune diseases. Myelin basic protein (MBP) peptide 1–11 induces experimental autoimmune encephalomyelitis (EAE) in susceptible strains of mice. Here we show that a herpesvirus Saimiri (HVS) peptide, AAQRRPSRPFA, with a limited homology to MBP1–11 peptide, ASQKRPSQRHG (underlined letters showing homology), can stimulate a panel of MBP1–11-specific T cell hybridomas and more importantly cause EAE in mice. We demonstrate that this is due to cross-recognition of these two peptides by TCRs. Results presented in this communication are the first demonstration that a viral peptide with homology at just 5 amino acids with a self peptide can induce clinical signs of EAE in mice. These findings have important implications in understanding the breakdown of T cell tolerance to self Ags in autoimmune diseases by means of cross-reactivity with unrelated peptides.

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