RORa enforces stability of the T-helper-17 cell effector program (RNA-Seq). RORa enforces stability of the T-helper-17 cell effector program (RNA-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: RNA-Seq: To investigate the molecular mechanism by which RORa regulates the Th17 program, TWT and TAKO Th17 cells were isolated from the DLN and SC of 3 separate cohorts of mixed chimeric mice based on their IL17AeGFP expression (see Figure 1G) at the peak of EAE disease, and their transcriptomes were sequenced (RNA-Seq)(Figures S3A-C).