Title : The IL17A and IL17F loci have divergent histone modifications and are differentially regulated by prostaglandin E2 in Th17 cells.

Pub. Date : 2013 Oct

PMID : 23800789






7 Functional Relationships(s)
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1 The IL17A and IL17F loci have divergent histone modifications and are differentially regulated by prostaglandin E2 in Th17 cells. Dinoprostone interleukin 17A Homo sapiens
2 Prostaglandin E2 (PGE2), IL-23 and IL-1beta are implicated in inflammatory bowel disease susceptibility, likely in part by modulating IL-17 producing CD4(+) T helper (Th17) cells. Dinoprostone interleukin 17A Homo sapiens
3 Prostaglandin E2 (PGE2), IL-23 and IL-1beta are implicated in inflammatory bowel disease susceptibility, likely in part by modulating IL-17 producing CD4(+) T helper (Th17) cells. Dinoprostone interleukin 17A Homo sapiens
4 To better understand how these three mediators affect Th17 cell memory responses, we characterized the gene expression profiles of activated human peripheral CD4(+) effector memory T cells and sorted Th17 memory cells from healthy donors concurrent with IL17A mRNA induction mediated by PGE2 and/or IL-23 plus IL-1beta. Dinoprostone interleukin 17A Homo sapiens
5 We discovered that PGE2 and IL-23 plus IL-1beta differentially regulate Th17 cytokine expression and synergize to induce IL-17A, but not IL-17F. Dinoprostone interleukin 17A Homo sapiens
6 The addition of PGE2 to IL-23 plus IL-1beta only enhances IL-17A expression as mediated by the PGE2 EP4 receptor, and promotes a switch from an IL-17F to an IL-17A predominant immune response. Dinoprostone interleukin 17A Homo sapiens
7 The addition of PGE2 to IL-23 plus IL-1beta only enhances IL-17A expression as mediated by the PGE2 EP4 receptor, and promotes a switch from an IL-17F to an IL-17A predominant immune response. Dinoprostone interleukin 17A Homo sapiens