Autoimmune diseases of myelin.
In this brief overview, I have identified some of the cardinal facts involving neuroantigens and neuroautoimmunologic responses to them, briefly listed the clinical-immunohistopathologic features of EAE, discussed the presence of circulating MBP degradation fragments in the blood of rats and humans and the high probability of some of these fragments serving to act as immunomodulating factors with respect to maintaining immunologic silence of varying numbers of MBP-reactive lymphoid cells in the blood and peripheral lymphoid tissues of clinically well humans. Perhaps more important is the inhibitory effect which such factors might well exert on expanding MBP-reactive clones of lymphocytes should they escape from immunological silence and become activated for one reason or another. The degree of concordance of immunological events and responses characterizing animals with EAE and patients with MS serves to underline the usefulness and the validity of the EAE animal model system for probing fundamental mechanisms implicated in the tissue injury characterizing the MS process.
D000818:Animals; D002457:Cell Extracts / Q000276:immunology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D005620:Freund's Adjuvant; D006801:Humans; D008221:Lymphoid Tissue / Q000276:immunology; D009103:Multiple Sclerosis / Q000276:immunology; D004676:Myelin Basic Protein / Q000097:blood / Q000276:immunology*; D011863:Radioimmunoassay / Q000379:methods; D051381:Rats; D013601:T-Lymphocytes / Q000276:immunology
D002457:Cell Extracts; D004676:Myelin Basic Protein; D005620:Freund's Adjuvant