Vulnerability of cell-surface receptors to autoimmune reactions.
A previous hypothesis in which myasthenia gravis was explained by an immune response to acetylcholine receptors has been validated, and is here extended to cell receptors in general. Receptors on target cells, being accessible to circulating trophic hormones or transmitters, must also be accessible to antibodies which compete with the natural mediator for access to the site. To detect anti-receptor antibodies, physiological assay systems would be more sensitive than conventional immunological assays. Autoimmune responses to receptor sites would require a genetic predisposition to failure of immunological tolerance such as occurs in various autoimmune diseases. This hypothesis is supported by recent findings in hyperthyroidism and a type of insulin-resistant diabetes mellitus, and is applicable to other endocrinopathies, diseases in which dysfunction at receptor sites can be postulated, and regulatory functions within the immune system itself.
D000818:Animals; D001323:Autoantibodies / Q000302:isolation & purification; D001327:Autoimmune Diseases; D001666:Binding Sites, Antibody; D002462:Cell Membrane / Q000276:immunology*; D003920:Diabetes Mellitus / Q000276:immunology / Q000473:pathology; D006801:Humans; D006980:Hyperthyroidism / Q000276:immunology / Q000473:pathology; D007108:Immune Tolerance; D066298:In Vitro Techniques; D008214:Lymphocytes / Q000276:immunology; D009157:Myasthenia Gravis / Q000276:immunology / Q000473:pathology; D011817:Rabbits; D011950:Receptors, Cholinergic; D011955:Receptors, Drug
D001323:Autoantibodies; D011950:Receptors, Cholinergic; D011955:Receptors, Drug