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• W2258354903 abstract "Abstract Genome-wide association studies (GWASs) for autoimmune diseases (ADs) have identified many risk loci and have provided insights into the etiology of each disease. Some of these loci, such as PTPN22 , IL23R and STAT4 , are shared among different ADs, and the combination of risk loci may determine an individual’s susceptibility for a disease. The majority of GWAS loci are expression quantitative trait loci (eQTLs), where disease-causing variants regulate expression of neighboring (or sometimes distant) genes. Because the eQTL effects are often cell type-specific, the incorporation of epigenetic data from disease-related cell types and tissues is expected to refine the identification of causal variants. The cumulative eQTL effects in multiple genes may influence the activity or fate of immune cells, which in turn may affect the function of the immune system in individuals. In this paper, I review the etiology of ADs by focusing on important immune cells (T h 1 cells, T h 17 cells and regulatory T cells), important pathways (antigen-receptor signaling and type I interferon signaling) and relevant genes identified in GWASs." @default.
• W2258354903 created "2016-06-24" @default.
• W2258354903 creator A5051943160 @default.
• W2258354903 date "2016-02-08" @default.
• W2258354903 modified "2023-10-16" @default.
• W2258354903 title "Genetics of autoimmune diseases: perspectives from genome-wide association studies" @default.
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• W2258354903 doi "https://doi.org/10.1093/intimm/dxw002" @default.
• W2258354903 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4889885" @default.
• W2258354903 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26857735" @default.
• W2258354903 hasPublicationYear "2016" @default.
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