This Research Topic is the second volume of the “Epigenetics of the Immune Component of Inflammation”. Please see the first volume
here.
Epigenetics refers to heritable changes in gene expression and function with no changes in DNA sequence, including modification of nucleotide sequences, post-translational modifications of proteins, and non-coding RNA (such as microRNA and LncRNA) expression. The mounting evidence suggests that epigenetic events may be involved in genesis of inflammation via modulating a variety of immune components such as cytokines, complements, antimicrobial peptides, cancer-related genes, and other inflammation-related genes. These epigenetic genes are constitutively activated or suppressed in a variety of immune- or non-immune cells under inflammatory conditions and incurred a variety of inflammatory diseases such as atherosclerosis, sepsis, diabetes, autoimmune disorders (rheumatoid arthritis, psoriasis, lupus erythematosus), neurodegenerative diseases, and cancer.
While there is evidence that the immune component of inflammation can result in epigenetic changes during genesis and development of inflammatory diseases, it is not always sure whether the immune component itself or the stimulated host cell is responsible for epigenetic changes. Moreover, although some epigenetic changes have been well characterized, their underlying mechanisms and origins are barely known. Given the importance of epigenetic function and plasticity in inflammatory diseases, the discovery and exploration of the roles of new epigenetic genes in the occurrence and development of inflammation via regulating immune components will contribute to develop effective new strategies for the diagnosis and treatment of inflammatory diseases.
Under this Research Topic, we welcome the Original Research Articles, Methods, and Reviews that explore the role of epigenetic changes in the occurrence and development of inflammatory diseases, and development of innovative epigenetic-based diagnostic and therapeutic strategies. The following direction are especially welcome:
(1) The detection of inflammation-induced epigenetic changes in the host immune system using genome-wide sequencing and/or targeted analysis.
(2) Identifying epigenetic genes and their mediated immunological signaling associated with inflammation including its occurrence and development.
(3) Mapping the cellular epigenetic networks driving susceptibility to inflammatory diseases using various omics analysis techniques.
(4) The potential action mechanisms of epigenetic modifications in inflammation during atherosclerosis, infection, rheumatism, rheumatoid arthritis, diabetes, neurodegenerative disease, and inflammation-related cancers.
(5) Development and differentiation of immune cells mediated by epigenetic genes.
(6) Targeting epigenetic genes to develop potential new agents against varieties of inflammation-related diseases.
