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J. Exp. Med.,
Volume 189, Number 8, April 19, 1999 1275-1284
By
From the * Department of Neurology and Neurological Sciences, Stanford University School of
Medicine, Stanford, California 94305; the Molecular mimicry refers to structural homologies between a self-protein and a microbial protein.
A major epitope of myelin basic protein (MBP), p87-99 (VHFFKNIVTPRTP), induces experimental autoimmune encephalomyelitis (EAE). VHFFK contains the major residues for binding of
this self-molecule to T cell receptor (TCR) and to the major histocompatibility complex. Peptides from papilloma virus strains containing the motif VHFFK induce EAE. A peptide from human papilloma virus type 40 (HPV 40) containing VHFFR, and one from HPV 32 containing
VHFFH, prevented EAE. A sequence from Bacillus subtilis (RKVVTDFFKNIPQRI) also prevented EAE. T cell lines, producing IL-4 and specific for these microbial peptides, suppressed EAE.
Thus, microbial peptides, differing from the core motif of the self-antigen, MBPp87-99, function
as altered peptide ligands, and behave as TCR antagonists, in the modulation of autoimmune disease.
Department of Immunology, The Weizmann Institute of
Science, Rehovot 76100, Israel; § Neurocrine Biosciences, Inc., San Diego, California 92121; and Epimmune, Inc., San Diego, California 92121
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