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[Pathogenesis of cutaneous lupus erythematosus from LE-prone mice].

Mouse models are similar but not identical to human diseases. However, they are important for research into the pathogenesis underlying autoimmune diseases because they allow us to evaluate similarities and differences between human diseases and mouse models. There are many inbred strains of systemic lupus erythematosus (SLE)-prone mice including New Zealand Black (NZB), F1 hybrids of NZB x New Zealand White (NZW) (B/W F1), MRL/Mp-lpr/lpr (MRL/lpr), and BXSB mice. The postulated etiology of these murine diseases includes many genetic and extrinsic factors such as retroviruses, an impaired balance of T cell interaction, ultraviolet irradiation, etc. For examples, genetic studies of MRL/lpr mice revealed that the appearance of macroscopic LE-like skin lesions needs the lpr mutation plus an additional factor in an autosomal dominant fashion. The candidate is ultraviolet (UV) B light, the susceptibility to which is regulated by the genetic background. Such abnormalities described in SLE now span the spectrum from innate immunity to acquired immunity. In this review, based on historical review, we focus on skin lesions from the well-studied MRL/lpr and B/W F1 mouse and discuss how SLE-prone mice can contribute to a better understanding of cutaneous LE pathogenesis.