Epigenetikk ved revmatoid artritt, med fokus på DNA-metylering av T-celler

BACKROUND: Rheumatoid arthritis (RA) is the most common autoimmune disease worldwide, affecting around 1 % of the population. Without aggressive treatment the disorder may cause major suffering and mortality. Epigenetic markers have been identified as potential mediators of genetic risk. Recent data suggest that epigenetic mechanisms communicate the effect of environmental factors in RA. Even though the investigation of DNA-methylation of T-cells has been limited, T-lymphocytes are considered the most important immunological effector cells in the disease, and pivotal in the pathogenesis of RA. Furthermore, genes of risk are identified in T-cells. OBJECTIVE: To investigate the epigenetics in RA, with a focus on DNA-methylation of Tcells. DATA SOURCES: A search was performed 20.12.16 in PubMed using the keywords “(Rheumatoid arthritis) AND DNA AND methylation AND T-cells”. METHOD: The search was limited to human case control studies with genome wide methylation analysis with a focus on phenotype (disposition for RA). RESULTS: Of 44 articles retrieved, three met the criteria. All three studies suggested differential methylation in T-cells from RA-patients compared with healthy controls. Two studies suggested dominance of non-island associated CpGs. Two genes (DUSP22 and GALNT9) were reported in more than one study, with methylation results of largest effect size. CONCLUSIONS: The present study is a limited basis to draw conclusions from, however, indications of differential methylation, and hyper- and hypomethylation of certain genes were found. The results encourage to do more and larger similar studies