Murine models of autoimmune disease and Sjouml;gren's syndrome

摘要

NA;Murine models of autoimmune disease exhibit heterogenous features that are now being understood in terms of their basic molecular defects. Defects in apoptosis genes or genes that contribute to Bhyphen;cell activation, Thyphen;cell tolerance loss, and development of autoimmune disease, including glomerulonephritis, have been identified. The interaction of primary and secondary predisposing genes leads to a diverse spectrum of autoimmune features that is different in different strains of mice. The challenge in the future will be to correlate these primary and secondary autoimmune genes with specific environmental triggers to explain the diverse spectrum of autoimmune disease. The ability to correct the apoptosis defect and autoimmune disease in CD2hyphen;Fastransgenic MRLhyphen;lprsol;lprmice brings hope that genetic therapy will eventually be possible in humans.Current Opinion in Rheumatology 1993,5colon;557hyphen;569