摘要: without appropriate animal models, although no single model perfectly mimics a human disease. Animal models are commonly used to study the genetic, environmental, and pathogenic aspects of autoimmune diseases. Regarding experimental diseases, these can be divided into several broad groups: (a) inbred mice that spontaneously develop disease similar systemic lupus erythematosus (SLE); (b) chronic graft-vs-host diseases induced in F1 hybrid injected with lymphoid parental cells; (c) ultraviolet (UV) light-irradiated immunized some components DNA; (d) immunodeficient such as severe combined (SCID) nude inoculated or engrafted immunocompetent cells tissues; (e) gene-manipulated transgenic knockout mice. There many strains SLE-prone mice, including New Zealand Black (NZB), hybrids NZB × White (NZW) (B/W F1), MRL/Mp-lpr/lpr (MRL/lpr), BXSB The postulated etiologic factors murine include retroviruses, thymic abnormalities, antithymocyte antibodies, polyclonal Bcell activation, an impaired balance T-cell interaction, abnormalities phagocytic (Andrews et al. 1978). Such described SLE now span spectrum from cellular immunology immunoglobulin idiotypes, cytokines, apoptosis, DNA repair, endogenous retroviruses (Steinberg 1995). Immunologic tolerance is revisited organ-specific (Nishimura Honjo 2001, Shimizu 2002). Based on trends, new important studies pathogenesis have been reported field internal organ biology, kidney, lung, salivary glands. In this review, based historical we focus skin lesions well-studied MRL/lpr B/W discuss how contribute better understanding cutaneous LE (CLE).