Altered oligosaccharides as the initiating autoantigen in rheumatoid arthritis.
The linkage of rheumatoid arthritis (RA) to infection though vague has remained a persistent notion for the past fifty years. The hypotheses that streptococcus was responsible; then M. Pneumoniae; the implication of a viral pathogenesis and, more especially, the Epstein-Barr virus, have all not withstood the test of Koch's postulates. Today, autoimmunity holds the field in the pathogenesis of RA. We know in fair detail what happens after failure of self-recognition develops. Why does synovial tissue become antigenic? Altered receptors of cell surface may be the loci of change, namely, glycoproteins and glycolipids. A hypothesis is constructed based on alteration by viral DNA of these cell surface markers that are then recognized as alien. Evidence is drawn from insulin dependent juvenile diabetes, glomerulonephritis, and Landsteiner blood groups. The initial lesion may be initiated by an infectious agent leading to a chain of events, the first link constituting change of the specific glycoprotein or glycolipid of a cell to one of antigenic challenge, thus stimulating an autoimmune reaction. The ultimate destructive-proliferative sequences of RA are then set in motion.
D000017:ABO Blood-Group System / Q000276:immunology; D000941:Antigens / Q000276:immunology*; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D001324:Autoantigens / Q000276:immunology*; D001327:Autoimmune Diseases / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology; D005921:Glomerulonephritis / Q000209:etiology / Q000276:immunology; D006017:Glycolipids / Q000276:immunology; D006023:Glycoproteins / Q000276:immunology; D006801:Humans; D009844:Oligosaccharides / Q000276:immunology*; D013290:Streptococcal Infections
D000017:ABO Blood-Group System; D000941:Antigens; D001324:Autoantigens; D006017:Glycolipids; D006023:Glycoproteins; D009844:Oligosaccharides