Transcription factor ID2 prevents E proteins from enforcing a naïve T lymphocyte gene program during NK cell development.
Transcription factor ID2 prevents E proteins from enforcing a naïve T lymphocyte gene program during NK cell development.
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DOI:
10.1126/sciimmunol.aao2139
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发表时间:
2018-04-27
影响因子:
24.8
通讯作者:
Kee BL
中科院分区:
文献类型:
--
作者:
Zook EC;Li ZY;Xu Y;de Pooter RF;Verykokakis M;Beaulieu A;Lasorella A;Maienschein-Cline M;Sun JC;Sigvardsson M;Kee BL
All innate lymphoid cells (ILC) require the small helix-loop-helix transcription factor ID2 but the functions of ID2 are not well understood in these cells. Here we show that mature natural killer (NK) cells, the prototypic ILC, 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 naïve T cells, and they transitioned from a CD8 memory-precursor-like to a naïve-like chromatin accessibility state. We demonstrate that ID3 was required for the development of ID2-deficient NK cells indicating that completely unfettered E protein function is incompatible with NK cell development. These data solidify the roles of ID2 and ID3 as mediators of effector and naïve gene programs, respectively, and revealed a critical role for ID2 in promoting a chromatin state and transcriptional program in CD27+CD11b− NK cells that supports cytotoxic effector differentiation and cytokine responses. NK cell maturation depends on transcription factor ID2 blocking acquisition of a naïve T cell gene program
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影响因子:
48
作者:
Langmead, Ben;Salzberg, Steven L.
通讯作者:
Salzberg, Steven L.
影响因子:
32.4
作者:
Dias, Sheila;Mansson, Robert;Gurbuxani, Sandeep;Sigvardsson, Mikael;Kee, Barbara L.
通讯作者:
Kee, Barbara L.
DOI:
10.4049/jimmunol.181.9.6394
发表时间:
2008-11-01
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Fodil-Cornu N;Lee SH;Belanger S;Makrigiannis AP;Biron CA;Buller RM;Vidal SM
通讯作者:
Vidal SM
影响因子:
64.5
作者:
Karo JM;Schatz DG;Sun JC
通讯作者:
Sun JC
影响因子:
4.8
作者:
Bayly, R;Chuen, L;LeBrun, DP
通讯作者:
LeBrun, DP