Kelsey Bennion, Brigham Young University
There has been extensive research into the field of epigenetics seeking new treatments for immune diseases. Autoimmune diseases, a branch of immune disease, are caused by a myriad of imbalances in the immune system. One of these imbalances is the overexpression of proinflammatory cytokines. The goal of this project was to examine epigenetic mechanisms of this overexpression. Because of the genetic similarity between humans and rhesus macaques, rhesus macaques may be a useful animal model for epigenetic regulation of inflammation. Our study focuses on the role of methylation in the promoter regions of candidate genes selected for their role in inflammatory immune pathways in 154 infant rhesus macaques. Plasma cytokines were quantified using ELISA and genome-wide methylation levels were quantified using restricted representation bisulfite sequencing (RRBS). ANOVA results revealed that the methylation of the IFNG2 gene influences expression in IL-6 (interleukin 6) and MCP1 (monocyte chemoattractant protein) (F(31,90)=2.490, p