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A gene network regulated by the transcription factor VGLL3 as a promoter of sex-biased autoimmune diseases.

Liang, Yun; Tsoi, Lam C; Xing, Xianying; Beamer, Maria A; Swindell, William R; Sarkar, Mrinal K; Berthier, Celine C; Stuart, Philip E; Harms, Paul W; Nair, Rajan P; Elder, James T; Voorhees, John J; Kahlenberg, J Michelle; Gudjonsson, Johann E.
Nat Immunol; 18(2): 152-160, 2017 02.
Artigo em Inglês | MEDLINE | ID: mdl-27992404
Autoimmune diseases affect 7.5% of the US population, and they are among the leading causes of death and disability. A notable feature of many autoimmune diseases is their greater prevalence in females than in males, but the underlying mechanisms of this have remained unclear. Through the use of high-resolution global transcriptome analyses, we demonstrated a female-biased molecular signature associated with susceptibility to autoimmune disease and linked this to extensive sex-dependent co-expression networks. This signature was independent of biological age and sex-hormone regulation and was regulated by the transcription factor VGLL3, which also had a strong female-biased expression. On a genome-wide level, VGLL3-regulated genes had a strong association with multiple autoimmune diseases, including lupus, scleroderma and Sjögren's syndrome, and had a prominent transcriptomic overlap with inflammatory processes in cutaneous lupus. These results identified a VGLL3-regulated network as a previously unknown inflammatory pathway that promotes female-biased autoimmunity. They demonstrate the importance of studying immunological processes in females and males separately and suggest new avenues for therapeutic development.
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