Animal models of spontaneous and drug-induced cutaneous lupus erythematosus

Skin lesions are one of the most common manifestations of lupus erythematosus (LE) disorders such as systemic LE and discoid LE. The etiology of cutaneous LE is not fully understood. To address this issue, appropriate animal models frequently clarify the etiology and pathogenesis of autoimmune diseases, although no single animal model perfectly mimics a human disease. A common dermatological finding in many SLE-prone mouse strains is the deposition of immunoglobulins at the dermoepidermal junction. Over the past decade, the most exciting and important finding has been the discovery of the Fas-defect in the pathogenesis of the autoimmune MRL/lpr mouse, which is a good model for the spontaneous development of skin lesions similar to those seen in human LE. The analysis of MRL/lpr mice showed a close association between immunoglobulin deposits and the appearance of skin lesions. Transgenic and knock out mice have advanced the investigation of cutaneous LE. Furthermore, the model of drug-induced cutaneous LE can yield additional insight since the trigger is clear in drug-induced LE. Cutaneous LE lesions can also be induced in TCRα−/− mice treated with fluorouracil and ultraviolet B light irradiation. Studies on both spontaneous and experimental models will elucidate the pathogenesis of complicated and multifactorial cutaneous LE.