RORa enforces stability of the T-helper-17 cell effector program (ChIP-Seq). RORa enforces stability of the T-helper-17 cell effector program (ChIP-Seq)

Chronic inflammation is responsible for a number of debilitating human diseases including inflammatory bowel disease, multiple sclerosis, and rheumatoid arthritis. The Th17 subset of T lymphocytes is an important player in the development of these pathogenic conditions. The transcription factor, RORgt was initially coined the master regulator of the Th17 program, but targeting RORgt therapeutically is dangerous owing to an enhanced risk of thymoma upon its inhibition. Another ROR family member, RORa, has also been implicated in Th17 function. Overall design: ChIP-Seq: To ascertain whether RORa directly regulates Th17 lineage maintenance, ChIP-Seq of RORa was performed with in vitro differentiated Th17 cells generated from RORa -Twin Strep (RORA-TS) tag knockin-in mice. To further address the interdependency of RORa and RORgt in binding of target loci, RORa ChIP-Seq was also conducted on Th17-polarized CD4+ T cells isolated from RORA-TS mice in which RORgt activity was abolished (RORA-TS-TGKO).