Epigenome-wide association data implicate DNA methylation as an intermediary of genetic risk in rheumatoid arthritis.

ABSTRACT: Epigenetic mechanisms integrate genetic and environmental causes of disease, but comprehensive genome-wide analyses of epigenetic modifications have not yet demonstrated robust association with common diseases. Using Illumina HumanMethylation450 arrays on 354 anti-citrullinated protein antibody-associated rheumatoid arthritis cases and 337 controls, we identified two clusters within the major histocompatibility complex (MHC) region whose differential methylation potentially mediates genetic risk for rheumatoid arthritis. To reduce confounding factors that have hampered previous epigenome-wide studies, we corrected for cellular heterogeneity by estimating and adjusting for cell-type proportions in our blood-derived DNA samples and used mediation analysis to filter out associations likely to

SUBMITTER: Liu Y 

PROVIDER: S-EPMC3598632 | biostudies-literature | 2013 Feb

REPOSITORIES: biostudies-literature