Interleukin-23-induced transcription factor Blimp1 promotes pathogenicity of T helper 17 cells

ABSTRACT: Interleukin-23 (IL-23) is a pro-inflammatory cytokine required for the pathogenicity of T helper 17 (Th17) cells but the molecular mechanisms governing this process remain unclear. We identified the transcription factor Blimp-1 (Prdm1) as a key IL-23-induced factor that drove the inflammatory function of Th17 cells. In contrast to thymic deletion of Blimp-1, which causes T cell development defects and spontaneous autoimmunity, peripheral deletion of this transcription factor resulted in reduced Th17 activation and reduced severity of autoimmune encephalomyelitis. Furthermore, genome wide occupancy and overexpression studies in Th17 cells revealed that Blimp-1 co-localized with transcription factors RORγt, STAT-3 and p300 at the Il23r, Il17a/f and Csf2 cytokine loci to enhance the

ORGANISM(S): Mus musculus

SUBMITTER: Yuka Kanno 

PROVIDER: E-GEOD-75724 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress