title: Animal models of molecular pathology systemic lupus erythematosus.
abstract: Systemic lupus erythematosus (SLE) is an autoimmune disease that affects multiple organ systems. A hallmark of SLE is the production of antinuclear antibodies against nuclear antigens such as chromatin and DNA. High levels of autoAbs promote the formation of immune complexes which can lead to the development of glomerulonephritis and progress to end-stage renal failure. Although the exact etiology of SLE is unknown, it is thought to be multifactorial in nature. A combination of environmental, hormonal, and a predisposed genetic background lead to the development of this disorder. Here, we review the various mouse models that have been used to study SLE and discuss how their study has led to a better understanding of the genetic and cellular factors involved in the development of systemic autoimmunity and lupus-like clinical symptoms. We also review the mouse studies that have explored the molecular pathways that are altered in this disease and the investigation of their therapeutic potentials.
authors.affiliation: Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, Florida, USA.
authors.forename: Allison
authors.initials: A
authors.lastname: Sang
authors.forename: Yiming
authors.initials: Y
authors.lastname: Yin
authors.forename: Ying-Yi
authors.initials: YY
authors.lastname: Zheng
authors.forename: Laurence
authors.initials: L
authors.lastname: Morel
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology / Q000473:pathology* / Q000628:therapy; D008285:Major Histocompatibility Complex / Q000276:immunology; D057089:Pathology, Molecular; D015398:Signal Transduction