Article
Deletion of the antiphospholipid syndrome autoantigen β2 -glycoprotein I potentiates the lupus autoimmune phenotype in a Toll-like receptor 7-mediated murine model.
Arthritis & rheumatology (Hoboken, N.J.) - 1 Aug 2014
Giannakopoulos Bill, Mirarabshahi Peyman, Qi Miao, Weatherall Chris, Qi Jian Cheng, Tanaka Kumiko, Millar Ewan, Vonthethoff Leon, Gatto Dominique, Spielman Derek, Krilis Steven A
Abstract excerpt
OBJECTIVE: The BXSB.Yaa mouse strain is a model of systemic lupus erythematosus that is dependent on duplication of the Toll-like receptor 7 gene. The objective of this study was to systematically describe the amplified autoimmune phenotype observed when the soluble plasma protein β2 -glycoprotein I (β2 GPI) gene was deleted in male BXSB.Yaa mice. METHODS: We generated BXSB.Yaa and NZW mouse strains in which the...
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