当前位置： SCI文献检索 > INTERNATIONAL IMMUNOPHARMACOLOGY期刊下所有文献 > Astilbin promotes the induction of regulatory NK1.1- CD4+ NKG2D+ T cells through the PI3K, STAT3, and MAPK signaling pathways.

Astilbin promotes the induction of regulatory NK1.1- CD4+ NKG2D+ T cells through the PI3K, STAT3, and MAPK signaling pathways.

Abstract：

:Astilbin is a potential agent for autoimmune and inflammatory diseases and has a protective effect in mice with DSS-induced colitis. NK1.1- CD4+ NKG2D+ T cells are a subpopulation of regulatory T cells that produce TGF-β1 and IL-10. Whether astilbin directly promotes the induction of NK1.1- CD4+ NKG2D+ T cells and whether these astilbin-stimulated T cells exert an immune-regulatory role remain unclear. Here, we show that astilbin efficiently induces the production of NK1.1- CD4+ NKG2D+ T cells with high expressions of TGF-β1, IL-10, CCR6, and CCR9 in a dose-dependent manner ex vivo. These regulatory T cells also substantially inhibit the activities of CD8+ T cells and macrophages. Intraperitoneal injection of astilbin ameliorates the severity of colitis with an increase in the frequency of NK1.1- CD4+ NKG2D+ T cells in the colon tissue of DSS-treated mice. Moreover, adoptive transfer of NK1.1- CD4+ NKG2D+ T cells induced by astilbin remarkably protects against the onset of DSS-induced colitis. Finally, the PI3K, STAT3, and MAPK signaling pathways are involved in the induction of NK1.1- CD4+ NKG2D+ T cells by astilbin. Taken together, our study elucidates a new immune-regulatory mechanism of astilbin by inducing the regulatory NK1.1- CD4+ NKG2D+ T cells and indicates a potential clinical use of astilbin for patients with inflammatory bowel diseases.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Han S,Lin Z,Wen J,Wu K,Xu Y,Zhang Y,Lu G,Xiao W,Ding Y,Jia X,Deng B,Gong W

doi

10.1016/j.intimp.2019.106143

subject

Has Abstract

pub_date

2020-04-01 00:00:00

pages

106143

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(19)32152-6

journal_volume

81

pub_type

杂志文章

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