Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells [ChIP-Seq experiments]

ABSTRACT: CD4+ T cells differentiate into phenotypically distinct T-helper cells upon antigenic stimulation. Regulation of plasticity between these CD4+ T-cell lineages is critical for immune homeostasis and prevention of autoimmune diseases. However, the factors that regulate lineage stability are largely unknown. Here we investigate a role for retinoic acid (RA) in the regulation of lineage stability using T helper 1 (Th1) cells, traditionally considered the most phenotypically stable Th subset. We found that RA, through its receptor RARa, sustains stable expression of Th1 lineage specifying genes as well as repressing genes that instruct Th17 cell fate. RA signaling is essential for limiting Th1 cell conversion into Th17 effectors and for preventing pathogenic Th17 responses in vivo. Our studies

ORGANISM(S): Mus musculus

SUBMITTER: Venu Pullabhatla 

PROVIDER: E-GEOD-60353 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress