Evidence for an immune complex disorder in systemic lupus erythematosus (SLE)

Abstract

Immunofluorescence findings have provided evidence for widespread immune complex deposits in SLE. Studies of severe proliferative lupus nephritis have shown that DNA-anti DNA complexes are of major importance. The immune complex systems in the deposits of mesangial and membranous lupus nephritis, as well as in extraglomerular sites have not been thoroughly analyzed, but there is evidence that antinuclear antibodies participate. The key role of DNA complexes in severe lupus nephritis (and probably in other lesions) may be due to its affinity for basement membranes. It is not clear to what extent immune complex deposits are initially formed in situ or as the result of arrest of circulating complexes; in any case, circulating complexes, which are present in high levels in patients with active SLE, are probably of crucial importance in SLE, since they can clearly form deposits in certain sites, add to existing deposits, saturate the reticuloendothelial system and exert other effects, such as on leucocyte function and the immune response. Other pathogenetic mechanisms are also of importance in SLE. In particular, autoantibodies against cell surface antigens can cause abnormalities of circulating cells and possibly parenchymal cells (as shown in studies on anti-brain antibodies). Experimental studies indicate that DTH reactions could account for some of the lesions of SLE, including glomerular lesions, but definitive evaluation of this mechanism awaits the development of techniques that allow positive identification of cell mediated reactions in vivo.