[Lupus erythematosus disseminatus, lesional mechanisms, pathogenesis and genetics].

Systemic lupus erythematosus (SLE) is a model of autoimmune disease. Its study, and that of spontaneous murine models, have benefited from new immunological and molecular biology techniques. New hypotheses have been put forward to explain the mechanisms of SLE lesions. The genetic origin of autoantibodies begins to be better known. Auxiliary CD4+ lymphocytes seem to play a capital role in the occurrence of lymphocyte abnormalities. The disease is multigenic. Much work is currently devoted to the identification and characterization of genetic factors.