期刊
CURRENT OPINION IN RHEUMATOLOGY
卷 26, 期 1, 页码 85-92出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/BOR.0000000000000012
关键词
CD4(+) memory T cells; genome-wide association studies; JAK-STAT signaling pathway; NF-B signaling pathway; regulatory T cells; rheumatoid arthritis
类别
资金
- National Institutes of Health (NIH) [R01-AR057108, R01-AR056768, U01-GM092691, R01-AR059648]
- Burroughs Wellcome Fund
- Japan Society of the Promotion of Science (JSPS)
Purpose of reviewA significant number of loci implicated in rheumatoid arthritis (RA) susceptibility have been highlighted by genome-wide association studies (GWAS). Here, we review the recent advances of GWAS in understanding the genetic architecture of RA, and place these findings in the context of RA pathogenesis.Recent findingsAlthough the interpretation of GWAS findings in the context of the disease biology remains challenging, interesting observations can be highlighted. Integration of GWAS results with cell-type specific gene expression or epigenetic marks have highlighted regulatory T cells and CD4(+) memory T cells as critical cell types in RA. In addition, many genes in RA loci are involved in the nuclear factor-kappaB signaling pathway or the Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling pathway. The observation that these pathways are targeted by several approved drugs used to treat the symptoms of RA highlights the promises of human genetics to provide insights in the disease biology, and help identify new therapeutic targets.SummaryThese findings highlight the promises and need of future studies investigating causal genes and underlined mechanisms in GWAS loci to advance our understanding of RA.
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