Pathogenesis of systemic lupus erythematosus.
SLE is a syndrome characterized by diverse clinical signs and symptoms, including rash, serositis, nephritis, central nervous system disease, thrombocytopenia, and leukopenia. These and other manifestations are present in patients with immune abnormalities indicative of B cell hyperactivity: hypergammaglobulinemia, increased amounts of antibodies reactive with self-determinants (characteristically including nuclear antigens), and increased numbers of circulating antibody-producing cells. It is this immune hyperactivity, inclusive of anti-self responses, which groups the patients with diverse clinical manifestations into a single syndrome called lupus.
D000818:Animals; D003165:Complement System Proteins / Q000235:genetics; D004198:Disease Susceptibility; D005796:Genes; D006801:Humans; D007107:Immune System / Q000502:physiology / Q000503:physiopathology; D007154:Immune System Diseases / Q000150:complications / Q000209:etiology / Q000503:physiopathology; D007130:Immunoglobulin Idiotypes / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000209:etiology* / Q000235:genetics; D051379:Mice; D008817:Mice, Mutant Strains / Q000235:genetics; D011951:Receptors, Complement / Q000235:genetics
D007130:Immunoglobulin Idiotypes; D011951:Receptors, Complement; D003165:Complement System Proteins