Recent progress towards elucidating the genetic basis for susceptibility to
systemic lupus erythematosus (SLE) has provided insights into the manner i
n which individual susceptibility genes contribute to disease pathogenesis.
Studies in animal models of systemic autoimmunity suggest that genes in th
ree separate pathways contribute to the initiation and progression of syste
mic autoimmunity. Linkage studies in humans suggest that at least some susc
eptibility genes mediating disease in lupus-prone mice may also contribute
to susceptibility in humans.