Genetic control of autoimmune disease: interactions between xid and Ipr.
A genetic experiment has been performed in mice to test the B cell "hyperactivity" hypothesis of autoantibody production. A backcross was designed such that some progeny carried both the sex-linked recessive gene xid, which markedly reduces the B cell hyperactivity and autoantibody production seen in NZB mice, and the autosomal recessive gene Ipr, which produces a severe lymphoproliferative/autoimmune disorder in the homozygous animal. The data indicate that although xid does not preclude any measured phenotypic expression of Ipr/Ipr disease, it may play a minor modulatory role. In addition, a background gene or genes in the CBA/N mouse, distinct from xid, modulates T cell proliferation in male backcross progeny. This experiment supports the view that autoimmune phenomena are fundamentally heterogeneous, and may involve complex cellular interactions.
D000818:Animals; D001327:Autoimmune Diseases / Q000235:genetics*; D002369:Castration; D003433:Crosses, Genetic; D005260:Female; D005808:Genes, Recessive; D014644:Genetic Variation; D008206:Lymphatic Diseases / Q000276:immunology; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D012730:Sex Chromosomes / Q000276:immunology*; D013739:Testosterone / Q000494:pharmacology; D013997:Time Factors
D013739:Testosterone