Genetic predisposition plays a crucial role in susceptibility to systemic l
upus erythematosus (SLE) in both human patients and animal models. Recent p
rogress in experimental systems and human linkage analysis is providing key
insights into the genetic basis for susceptibility and elucidating the man
ner in which genetic interactions mediate severe disease pathogenesis. Gene
s in multiple pathways appear to participate in specific elements of the di
sease, and epistatic interactions among these genes play an important role
in both aggravating and suppressing disease development.