当前位置： SCI文献检索 > CELLULAR SIGNALLING期刊下所有文献 > Early growth response genes 2 and 3 induced by AP-1 and NF-κB modulate TGF-β1 transcription in NK1.1- CD4+ NKG2D+ T cells.

Early growth response genes 2 and 3 induced by AP-1 and NF-κB modulate TGF-β1 transcription in NK1.1- CD4+ NKG2D+ T cells.

Abstract：

:NK1.1- CD4+ NKG2D+ T cells are a subpopulation of regulatory T cells that downregulate the functions of CD4+ T, CD8+ T, natural killer (NK) cells, and macrophages through TGF-β1 production. Early growth response genes 2 (Egr2) and 3 (Egr3) maintain immune homeostasis by modulating T lymphocyte development, inhibiting effector T cell function, and promoting the induction of regulatory T cells. Whether Egr2 and Egr3 directly regulate TGF-β1 transcription in NK1.1- CD4+ NKG2D+ T cells remains elusive. The expression levels of Egr2 and Egr3 were higher in NK1.1- CD4+ NKG2D+ T cells than in NK1.1- CD4+ NKG2D- T cells. Egr2 and Egr3 expression were remarkably increased after stimulating NK1.1- CD4+ NKG2D+ T cells with sRAE or α-CD3/sRAE. The ectopic expression of Egr2 or Egr3 resulted in the enhancement of TGF-β1 expression, while knockdown of Egr2 or Egr3 led to the decreased expression of TGF-β1 in NK1.1- CD4+ NKG2D+ T cells. Egr2 and Egr3 directly bound with the TGF-β1 promoter as demonstrated by the electrophoretic mobility shift assay and dual-luciferase gene reporter assay. Furthermore, the Egr2 and Egr3 expression of NK1.1- CD4+ NKG2D+ T cells could be induced by the AP-1 and NF-κB transcriptional factors, but had no involvement with the activation of NF-AT and STAT3. In conclusion, Egr2 and Egr3 induced by AP-1 and NF-κB directly initiate TGF-β1 transcription in NK1.1- CD4+ NKG2D+ T cells. This study indicates that manipulating Egr2 and Egr3 expression would potentiate or alleviate the regulatory function of NK1.1- CD4+ NKG2D+ T cells and this strategy could be used in the therapy for patients with autoimmune diseases or tumor.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Han S,Zhu T,Ding S,Wen J,Lin Z,Lu G,Zhang Y,Xiao W,Ding Y,Jia X,Chen H,Gong W

doi

10.1016/j.cellsig.2020.109800

subject

Has Abstract

pub_date

2020-12-01 00:00:00

pages

109800

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(20)30277-1

journal_volume

76

pub_type

杂志文章

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