Bhlhe40 mediates tissue-specific control of macrophage proliferation in homeostasis and type 2 immunity.
Ontology highlight
ABSTRACT: Most tissue-resident macrophage populations develop during embryogenesis, self-renew in the steady state and expand during type 2 immunity. Whether shared mechanisms regulate the proliferation of macrophages in homeostasis and disease is unclear. Here we found that the transcription factor Bhlhe40 was required in a cell-intrinsic manner for the self-renewal and maintenance of large peritoneal macrophages (LPMs), but not that of other tissue-resident macrophages. Bhlhe40 was necessary for the proliferation, but not the polarization, of LPMs in response to the cytokine IL-4. During infection with the helminth Heligmosomoides polygyrus bakeri, Bhlhe40 was required for cell cycling of LPMs. Bhlhe40 repressed the expression of genes encoding the transcription factors c-Maf and Mafb and directly
SUBMITTER: Jarjour NN
PROVIDER: S-EPMC6531324 | biostudies-literature | 2019 Jun
REPOSITORIES: biostudies-literature
ACCESS DATA