Furthermore, CREMα affects epigenetic modifications and transcriptional control of cytokines from the IL-17 family, namely IL17A and IL17F [32,44]. Both gene products, IL-17A and IL-17F, are strongly proinflammatory and are produced by T lymphocytes, natural killer cells, mast cells, and neutrophils [45]. Excessive IL-17 expression has been linked to several autoimmune diseases, including rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, and SLE [46–51]. The human IL17A and IL17F genes are located in close proximity to each other on chromosome 6 (within approximately 85 kb). Although the biological properties and regulation of IL-17F are less well studied than IL-17A, some information is available. It was recently demonstrated that increased CREMα expression in SLE T cells contributes to epigenetic remodeling of the IL17A/F gene locus. In SLE T cells recruitment of CREMα to the IL17A and the IL17F promoters is increased, as compared with T cells from healthy individuals. In contrast to the effects observed at the IL2 gene locus, CREMα recruits less HDAC1 and DNMT3a to the IL17A promoter, contributing to an overall increase in histone H3 acetylation and reduced histone
