期刊
IMMUNOLOGICAL REVIEWS
卷 294, 期 1, 页码 188-204出版社
WILEY
DOI: 10.1111/imr.12827
关键词
arthritis; genetics; polygenic; rheumatoid; statistical
类别
资金
- National Institute of Allergy and Infectious Diseases [U19AI111224]
- National Institute of Arthritis and Musculoskeletal and Skin Diseases [1R01AR063759, UH2AR067677]
- National Human Genome Research Institute [T32 HG002295]
Rheumatoid arthritis (RA) risk has a large genetic component (similar to 60%) that is still not fully understood. This has hampered the design of effective treatments that could promise lifelong remission. RA is a polygenic disease with 106 known genome-wide significant associated loci and thousands of small effect causal variants. Our current understanding of RA risk has suggested cell-type-specific contexts for causal variants, implicating CD4 + effector memory T cells, as well as monocytes, B cells and stromal fibroblasts. While these cellular states and categories are still mechanistically broad, future studies may identify causal cell subpopulations. These efforts are propelled by advances in single cell profiling. Identification of causal cell subpopulations may accelerate therapeutic intervention to achieve lifelong remission.
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