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Advances in genetics toward identifying pathogenic cell states of rheumatoid arthritis.

ABSTRACT: Rheumatoid arthritis (RA) risk has a large genetic component (~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.

SUBMITTER: Amariuta T

PROVIDER: S-EPMC7047592 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Advances in genetics toward identifying pathogenic cell states of rheumatoid arthritis.

Amariuta Tiffany T Luo Yang Y Knevel Rachel R Okada Yukinori Y Raychaudhuri Soumya S

Immunological reviews 20191128 1

Rheumatoid arthritis (RA) risk has a large genetic component (~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 ...[more]

PMID: 31782165

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