A number of mouse models have been utilized to study the pathophysiology of
immune complex (IC) disease, and the hallmark IC disease systemic lupus er
ythematosus (SLE). Many of these studies have provided exciting new insight
s into IC-mediated inflammation and autoimmunity. However, numerous differe
nces exist between mice and humans that suggest that mouse studies are not
always applicable to human disease. These differences can be found in the b
iological systems that interact with circulating TC, in the specifics of di
sease presentation, and in the general physiology of the two species. Furth
ermore, although the mechanisms of SLE-like autoimmune disease in the mouse
are being defined through analyses of the murine models of SLE, it remains
to be proven that these mechanisms are relevant to human SLE. Thus, genera
lizing the results of the mouse studies to human SLE and other human IC dis
eases must be done with caution.