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.
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19 April 1999
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April 19 1999
Microbial Epitopes Act as Altered Peptide Ligands to Prevent Experimental Autoimmune Encephalomyelitis
Pedro J. Ruiz,
Pedro J. Ruiz
From the *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305; the ‡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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Hideki Garren,
Hideki Garren
From the *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305; the ‡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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David L. Hirschberg,
David L. Hirschberg
From the *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305; the ‡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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Annette M. Langer-Gould,
Annette M. Langer-Gould
From the *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305; the ‡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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Mia Levite,
Mia Levite
From the *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305; the ‡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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Marcela V. Karpuj,
Marcela V. Karpuj
From the *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305; the ‡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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Scott Southwood,
Scott Southwood
From the *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305; the ‡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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Alessandro Sette,
Alessandro Sette
From the *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305; the ‡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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Paul Conlon,
Paul Conlon
From the *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305; the ‡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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Lawrence Steinman
Lawrence Steinman
From the *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305; the ‡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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Pedro J. Ruiz,
Hideki Garren,
David L. Hirschberg,
Annette M. Langer-Gould,
Mia Levite,
Marcela V. Karpuj,
Scott Southwood,
Alessandro Sette,
Paul Conlon,
Lawrence Steinman
From the *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305; the ‡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
Address correspondence to Lawrence Steinman, Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305-5316. Phone: 650-725-6401; Fax: 650-725-0627; E-mail: [email protected]
Received:
November 18 1998
Revision Received:
February 02 1999
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1999
J Exp Med (1999) 189 (8): 1275–1284.
Article history
Received:
November 18 1998
Revision Received:
February 02 1999
Citation
Pedro J. Ruiz, Hideki Garren, David L. Hirschberg, Annette M. Langer-Gould, Mia Levite, Marcela V. Karpuj, Scott Southwood, Alessandro Sette, Paul Conlon, Lawrence Steinman; Microbial Epitopes Act as Altered Peptide Ligands to Prevent Experimental Autoimmune Encephalomyelitis . J Exp Med 19 April 1999; 189 (8): 1275–1284. doi: https://doi.org/10.1084/jem.189.8.1275
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