Interplay between genetic and epigenetic mechanisms in rheumatoid arthritis
作者： Mojca Frank-Bertoncelj , Kerstin Klein , Steffen Gay
关键词: Transcriptome 、 Biology 、 DNA methylation 、 Epigenetics 、 Epigenome 、 Chromosome conformation capture 、 Genetics 、 Chromatin 、 Genome-wide association study 、 Cellular differentiation
摘要: Genetic and environmental factors contribute to the risk for rheumatoid arthritis (RA), with epigenetics serving as a possible interface through which RA. High-throughput technologies interrogating genome epigenome, availability of genetic epigenetic datasets across diversity cell types, enable identification candidate causal variants RA study their function in core processes. To date, were studied immune cells but not joint resident cells, example, synovial fibroblasts. Synovial fibroblasts from different joints are distinct, anatomically specialized defined by joint-specific transcriptomes, epigenomes phenotypes. Cell type-specific analysis changes, together fine mapping interrogation chromatin 3D interactions may identify new disease relevant pathways, potential therapeutic targets biomarkers progression or therapy response.
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