Chronic exposure to TGFβ1 regulates myeloid cell inflammatory response in an IRF7-dependent manner.

ABSTRACT: Tissue microenvironment influences the function of resident and infiltrating myeloid-derived cells. In the central nervous system (CNS), resident microglia and freshly recruited infiltrating monocyte-derived macrophages (mo-MΦ) display distinct activities under pathological conditions, yet little is known about the microenvironment-derived molecular mechanism that regulates these differences. Here, we demonstrate that long exposure to transforming growth factor-β1 (TGFβ1) impaired the ability of myeloid cells to acquire a resolving anti-inflammatory phenotype. Using genome-wide expression analysis and chromatin immunoprecipitation followed by next-generation sequencing, we show that the capacity to undergo pro- to anti-inflammatory (M1-to-M2) phenotype switch is controlled by the transcrip

SUBMITTER: Cohen M 

PROVIDER: S-EPMC4282639 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature