Transcription factor ID2 prevents E proteins from enforcing a naive T lymphocyte gene program during NK cell development.

ABSTRACT: All innate lymphoid cells (ILCs) require the small helix-loop-helix transcription factor ID2, but the functions of ID2 are not well understood in these cells. We show that mature natural killer (NK) cells, the prototypic ILCs, developed in mice lacking ID2 but remained as precursor CD27⁺CD11b^- cells that failed to differentiate into CD27^-CD11b⁺ cytotoxic effectors. We show that ID2 limited chromatin accessibility at E protein binding sites near naïve T lymphocyte-associated genes including multiple chemokine receptors, cytokine receptors, and signaling molecules and altered the NK cell response to inflammatory cytokines. In the absence of ID2, CD27⁺CD11b^- NK cells expressed ID3, a helix-loop-helix protein associated with naï

SUBMITTER: Zook EC 

PROVIDER: S-EPMC6750718 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature