Autoimmunity: present concepts.
Autoimmune disease may be effected by humoral mechanisms (direct antibody effect or pathogenic antigen-antibody complexes), cell-mediated mechanisms, and possibly complement in the absence of antibody. In view of recent work, self-tolerance can no longer be explained by the clonal selection theory; cells that are capable of recognizing self-antigens and effecting an autoimmune response seem to be present in the normal individual but actively regulated by a process involving antigen-antibody complexes or suppressor T cells. The determination that a clinical state is an autoimmune disease cannot, therefore, be made only on the basis of the presence of autoantibody as this may be part of the normal and active state of immunoregulation of autoimmunity. Indeed, the absence of autoantibody may be the immunodeficient state that allows a full-blown autoimmune disease to occur. In view of this knowledge, the basis for the diagnosis of autoimmune disease and the rationale for treatment based on the objective of inhibiting all immune responses to the autoantigen require re-examination.
D000818:Animals; D000917:Antibody Formation; D000921:Antibody-Producing Cells / Q000276:immunology; D000936:Antigen-Antibody Complex; D001323:Autoantibodies; D001327:Autoimmune Diseases / Q000276:immunology / Q000628:therapy; D001402:B-Lymphocytes / Q000276:immunology; D002465:Cell Movement; D003165:Complement System Proteins; D005260:Female; D006801:Humans; D007109:Immunity; D007111:Immunity, Cellular; D007153:Immunologic Deficiency Syndromes / Q000276:immunology; D007962:Leukocytes / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology; D011247:Pregnancy; D013601:T-Lymphocytes / Q000276:immunology
D000936:Antigen-Antibody Complex; D001323:Autoantibodies; D003165:Complement System Proteins