title: The pathogenesis of systemic lupus erythematosus.
abstract: Many investigators believe that systemic lupus erythematosus is an autoimmune disease, perhaps caused by inadequate suppressor T lymphocyte activity, which permits the activation of autoantibody producing B lymphocytes. This paper discusses the testable hypothesis that a superoxide-generating, chromosome aberration-inducing factor (clastogenic factor), present in the lymphocytes of lupus patients but absent from normals, is responsible for such a suppressor cell defect. Superoxide or activated oxygen species derived from it, such as hydroxyl radical, may be the molecular mediators of CF activity.
mesh_terms: D002869:Chromosome Aberrations; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000209:etiology*; D009153:Mutagens / Q000097:blood; D010100:Oxygen / Q000096:biosynthesis*; D013481:Superoxides / Q000096:biosynthesis*; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects*; D014466:Ultraviolet Rays / Q000009:adverse effects
chemical_list: D009153:Mutagens; D013481:Superoxides; D010100:Oxygen