Type 1 Diabetes (T1D) is a complex autoimmune disease affecting more than 30 million people worldwide. T1D is caused by a combination of genetic and epigenetic factors leading to immune destruction of insulin-secreting islet cells. Although significant progress has recently been made in elucidating the genetics of T1D, the non-genetics component has remained poorly defined. Multiple lines of evidence including studies of migrant populations and monozygotic twin pair discordance for T1D underline the role of epigenetic factors in this disease. Thus, the characterization of epigenome is critical for the development of new T1D therapeutics and for appropriate staging of disease. DNA methylation is one of the main epigenetic modifications involved in human disease. Using epigenome-wide analysis such as reduced representation bisulfite sequencing (RRBS), we aim to identify unique differentially methylated regions (DMRs) within the genome that accumulate in PBMCs isolated from circulating blood, that may reflect the immune insult that occurs with T1D onset. Then we are interested to study the role of these hypo or hyper methylated regions in T1D.
