Mechanisms of cutaneous tissue damage in lupus erythematosus

Abstract

Cutaneous disease in lupus is clinically heterogeneous, and it is likely that mechanisms of disease are also heterogeneous. Nevertheless, in many cutaneous forms of lupus and in the systemic disease itself, there is compelling evidence that autoantibodies are involved. It is our belief that autoantibodies are of primary importance in the etiology of the cutaneous lupus lesions discussed in this chapter and that antibody specificities are critical in most cases in determining the clinical expression of disease. As discussed earlier, antibodies can effect tissue injury by several mechanisms. There is evidence that ADCC may be an important mechanism of keratinocyte cytotoxicity in cutaneous lesions characterized by antibody deposition and a mononuclear cell infiltrate. Vasculitic lesions that have an infiltrate of polymorphonuclear cells may be related to antibody- and complement-dependent neutrophil-mediated endothelial cytotoxicity. Ultraviolet light, sex steroids, and certain genes such as those of the major histocompatibility complex appear to be important modulating factors in lupus.