Obata, Y., Furusawa, Y. & Hase, K. Epigenetic modifications of the immune system in health and disease. Immunol Cell Biol 93, 226–232 (2015).

This review paper details the effects that epigenetic modifications have on overall human health. The paper talk about histone modification and DNA methylation.
The informational parts of this review paper have been noted and I will be writing about the parts of the paper dealing with the connections between DNA methylation and proper immune regulation.
     Cited research found connections between  DNA methylation  (mouse model) and the homeostasis of Treg cells in the colon. The knock out of a certain cell responsible for DNA methylation maintenance, leads to a mis-development of functional Treg cells, leading to a increased inflammatory response and the development of severe colitis in the KO mice.
Additionally, DNA methylation is crucial to in the initial stages of Intestinal Epithelial Cells(IECs) when they are Intestinal Stem Cells(ISCs) before differentiation. Lack of DMNTs in a mouse model led to a lack of differentiated IECs, which serves as a balance point for a healthy mucosal barrier between the gut lumen and commensal gut bacteria.
Additionally, the paper cites several studies that demonstrate the capacity for infectious agents to alter the epigenetic status of normally function host cells, including E.coli and H. pylori.
     The review paper did fair job at giving a detailed background for the connections between gut mediated immunity, infectious agents and functional differentiation of IECs from ISCs. I will be reviewing the results of the cited papers that look at these specific effects. With regards to my overall project, this paper provides an additional pathway DNA methylation is connected with CRC risk. The overarching goal is to use big data approaches to combine multiple datasets in order to make connections between gut microbiota, DNA methylation and other clinical metadata. The information from this paper connects DNA methylation with environments conducive with carcinogenesis, including local inflammation and inflammatory gastrointestinal diseases.