GSE80375 | Datasets2Tools

General Information

Accession	GSE80375
Title	Cyclic AMP-responsive element-binding protein (CREB) is critical in autoimmunity by promoting Th17 but inhibiting Treg differentiation
Description	The molecular mechanisms that govern differential T cell development into pro-inflammatory Th17 vs. regulatory T (Treg) cells remain unclear. Here, we show that selective deletion of CREB in T cells or Th17 cells impaired Th17 differentiation in vitro and in vivo, and led to resistance to autoimmune diseases. Mechanistically, CREB, activated by CD3-PKC- signaling, plays a key role in regulating Th17 differentiation, at least in part through directly binding to the Il17-Il17f gene locus. Unexpectedly, although dispensable for FOXP3 expression and for the homeostasis and function of thymus-derived Treg cells, CREB negatively regulates the survival of TGF--induced Treg cells, and deletion of CREB resulted in increased FOXP3+ Treg cells in the intestine and protection in a colitis model. Thus, CREB is critical in autoimmune diseases by promoting Th17 and inhibiting de novo Treg generation.
Landing Page	https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80375
Repository	Gene Expression Omnibus