An inherently bi-functional subset of Foxp3+ Treg/T-helper cells is controlled by the transcription factor Eos

ABSTRACT: At sites of inflammation, certain Foxp3+ Tregs have the ability to alter their phenotype and become pro-inflammatory helper/effector cells, without losing Foxp3 expression. We show that this functional reprogramming is controlled by the transcription factor Eos (Ikzf4), an obligate co-repressor for Foxp3. The ability to reprogram was restricted to a specific subset of Foxp3+ Tregs, arising as early as the thymus and identifiable by short half-life of Eos at rest, characteristic cell-surface markers (CD38+CD69+CD103NEG) and a distinct pattern of DNA methylation. Mice made selectively deficient in this subset of Eos-labile Tregs became markedly impaired in their ability to cross-present new antigens and prime CD8+ T cells. Downregulation of Eos and consequent Treg reprogramming was preve

ORGANISM(S): Mus musculus

SUBMITTER: Huidong Shi 

PROVIDER: E-GEOD-44380 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress