Genetic Contributions to Lupus‐like Disease in (NZB×NZW)F1 Mice

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown etiology, characterized by the involvement of multiple organ systems and expression of diverse clinical manifestations. The hallmark of SLE is the production of autoantibodies directed against nuclear components, including ssDNA, dsDNA, and histones. Nearly 90% of lupus patients are female, with incidence increasing during childbearing years and decreasing after menopause [reviewed in (Kotzin & O'Dell 1994)]. For males, peak incidence may not be until the 7th decade of life. These data suggest a role for sex hormones in the development of disease, with estrogens exerting an enhancing effect and androgens a protective influence. The clinical course of patients with SLE is extremely variable. Some patients have mild forms of disease, with spontaneous remissions and regressions; others demonstrate low levels of skin and joint involvement and respond favorably to nonsteroidal anti-inflammatory medications. Still other patients follow a more relentless course, progressing to end organ damage (such as renal failure) frequently with multisystem involvement, in a manner unresponsive to high doses of corticosteroids and cytotoxic drugs.

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