Suppression of autoimmunity via microbial mimics of altered peptide ligands.
Molecular mimics of self-antigens can behave as altered peptide ligands and serve to ameliorate autoimmune disease. Analysis of experimental autoimmune encephalomyelitis with proteomic autoantibody microarrays reveals that there might exist a wide variety of microbes with features that mimic self-epitopes. Autoimmunity could therefore be modulated via microbial immunity, which may account for relapse and remission of ongoing disease.
Steinman
L
L
Dept of Neurological Sciences and Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine B002, Stanford University School of Medicine, CA 94305, USA. steinman@stanford.edu
Utz
P J
PJ
Robinson
W H
WH
D000818:Animals; D001324:Autoantigens; D015551:Autoimmunity; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000209:etiology / Q000276:immunology; D000939:Epitopes; D006801:Humans; D008024:Ligands; D051379:Mice; D018716:Molecular Mimicry / Q000276:immunology*; D009103:Multiple Sclerosis / Q000209:etiology / Q000276:immunology; D004676:Myelin Basic Protein / Q000276:immunology; D018991:Myelin Proteolipid Protein / Q000276:immunology; D010446:Peptide Fragments / Q000276:immunology; D010455:Peptides / Q000276:immunology*; D017634:Self Tolerance
D001324:Autoantigens; D000939:Epitopes; D008024:Ligands; D004676:Myelin Basic Protein; D018991:Myelin Proteolipid Protein; D010446:Peptide Fragments; D010455:Peptides; C107908:myelin basic protein 85-99; C435023:myelin proteolipid protein (139-151)