Interleukin 2, T cell receptor and sex hormone studies in autoimmune mice.
Systemic lupus erythematosus (SLE) is a disease of immune dysregulation in which B cell hyperactivity and T cell deficiency are important characteristics. Sex factors also play a major role in the pathogenesis based on the physiologic effects of estrogen in promoting immunologic hyperactivity. Our findings suggest that a posttranscriptional mechanism is responsible for the functional interleukin 2 (IL-2) defect since transcription of the IL-2 message occurs after mitogenic stimulation. The proliferating cell in the MRL/lpr mouse model of lupus may be an immature T cell. The T cell receptor in these mice has a lower molecular weight than normal. This aberrant T cell receptor might be explained by a defect in glycosylation. The administration of estrogen to pregnant mice late in gestation results in offspring with a permanently altered immune system. These mice develop features of autoimmunity similar to those that occur spontaneously in genetically susceptible autoimmune mice. This phenomenon may have etiopathological significance for familial SLE.
D000818:Animals; D001323:Autoantibodies / Q000235:genetics; D001402:B-Lymphocytes / Q000276:immunology; D005786:Gene Expression Regulation; D012739:Gonadal Steroid Hormones / Q000502:physiology*; D007376:Interleukin-2 / Q000235:genetics*; D008180:Lupus Erythematosus, Systemic / Q000235:genetics* / Q000276:immunology; D051379:Mice; D008815:Mice, Inbred Strains; D011948:Receptors, Antigen, T-Cell / Q000235:genetics*; D011971:Receptors, Immunologic / Q000235:genetics; D015375:Receptors, Interleukin-2; D013601:T-Lymphocytes / Q000276:immunology; D014158:Transcription, Genetic
D001323:Autoantibodies; D012739:Gonadal Steroid Hormones; D007376:Interleukin-2; D011948:Receptors, Antigen, T-Cell; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2