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Interplay between genetic and epigenetic mechanisms in rheumatoid arthritis


Frank-Bertoncelj, Mojca; Klein, Kerstin; Gay, Steffen (2017). Interplay between genetic and epigenetic mechanisms in rheumatoid arthritis. Epigenomics, 9(4):493-504.

Abstract

Genetic and environmental factors contribute to the risk for rheumatoid arthritis (RA), with epigenetics serving as a possible interface through which risk factors contribute to RA. High-throughput technologies for interrogating genome and epigenome, and the availability of genetic and epigenetic datasets across a diversity of cell types, enable the identification of candidate causal genetic variants for RA to study their function in core RA processes. To date, RA risk variants were studied in the immune cells but not joint resident cells, for example, synovial fibroblasts. Synovial fibroblasts from different joints are distinct, anatomically specialized cells, defined by joint-specific transcriptomes, epigenomes and phenotypes. Cell type-specific analysis of epigenetic changes, together with genetic fine mapping and interrogation of chromatin 3D interactions may identify new disease relevant pathways, potential therapeutic targets and biomarkers for RA progression or therapy response.

Abstract

Genetic and environmental factors contribute to the risk for rheumatoid arthritis (RA), with epigenetics serving as a possible interface through which risk factors contribute to RA. High-throughput technologies for interrogating genome and epigenome, and the availability of genetic and epigenetic datasets across a diversity of cell types, enable the identification of candidate causal genetic variants for RA to study their function in core RA processes. To date, RA risk variants were studied in the immune cells but not joint resident cells, for example, synovial fibroblasts. Synovial fibroblasts from different joints are distinct, anatomically specialized cells, defined by joint-specific transcriptomes, epigenomes and phenotypes. Cell type-specific analysis of epigenetic changes, together with genetic fine mapping and interrogation of chromatin 3D interactions may identify new disease relevant pathways, potential therapeutic targets and biomarkers for RA progression or therapy response.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Rheumatology Clinic and Institute of Physical Medicine
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:21 March 2017
Deposited On:28 Mar 2017 12:40
Last Modified:19 Feb 2018 07:48
Publisher:Future Medicine
ISSN:1750-1911
OA Status:Closed
Publisher DOI:https://doi.org/10.2217/epi-2016-0142
PubMed ID:28322583

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