Genome-wide DNA methylation patterns in CD4+ T cells from Chinese Han patients with rheumatoid arthritis

Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic inflammation of the joints. Recent evidence indicated the epigenetic changes may contribute to the pathogenesis of RA.

To understand the extent and nature of dysregulated DNA methylation in RA CD4T cells, we performed a genome-wide DNA methylation study in CD4 + T cells in 12 RA patients compared to 12 matched normal healthy controls. Cytosine methylation status was quantified with Illumina methylation 450K microarray.

The DNA methylation profiling showed 383 hyper- and 785 hypo-methylated genes in the CD4 + T cells of the RA patients (p < 3.4 × 10^-7). Gene ontology analysis indicated transcript alternative splicing and protein modification mediated by DNA methylation might play an important role in the pathogenesis of RA. In addition, the result showed that human leukocyte antigen (HLA) region including HLA-DRB6, HLA-DQA1 and HLA-E was frequently hypomethylated, but HLA-DQB1 hypermethylated in CpG island region and hypomethylated in CpG shelf region in RA patients. Outside the MHC region, HDAC4, NXN, TBCD and TMEM61 were the most hypermethylated genes, while ITIH3, TCN2, PRDM16, SLC1A5 and GALNT9 are the most hypomethylated genes.

Genome-wide DNA methylation profile revealed significant DNA methylation change in CD4 + T cells from patients with RA.