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中性粒细胞与 CD4+CD25+T 调节性细胞的相互作用:感染性耐受的一种可能新机制。

Neutrophil--CD4+CD25+ T regulatory cell interactions: a possible new mechanism of infectious tolerance.

机构信息

Department of Periodontology and Oral Mucosal Diseases, Medical University of Lodz, Lodz, Poland.

出版信息

Immunobiology. 2013 Apr;218(4):455-64. doi: 10.1016/j.imbio.2012.05.029. Epub 2012 Jun 7.

DOI:10.1016/j.imbio.2012.05.029
PMID:22749980
Abstract

This study tested the hypothesis that CD4(+)CD25(+)CD127(low) regulatory T (Treg) cells might induce immunosuppressive properties in apoptotic neutrophils. Treg cells are recognized as a major subset of immune cells possessing potent suppressive properties directed at T effector cells. However, Treg cells have recently been found to inhibit neutrophil function and promote their apoptosis. One of the mechanisms of action of Treg cells is the induction of other suppressor cell populations according to an infectious tolerance model. We showed that LPS-activated Treg cells promote generation of IL-10 and TGF-β1, inhibit IL-6 production by PMNs and induce the expression of heme oxygenase-1 (HO-1) and the suppressor of cytokine signaling 3 molecule (SOCS3). However, CD3/CD28-activated Treg cells were seen to promote TGF-β1 production, as well as IDO and HO-1 expression by PMNs. These findings suggest that Treg cells might play an important role in the direct control of innate immune responses through the induction of neutrophils with immunosuppressive properties that generate IL-10, TGF-β1, IDO and HO-1.

摘要

本研究旨在验证以下假设

CD4(+)CD25(+)CD127(low) 调节性 T (Treg) 细胞可能在凋亡中性粒细胞中诱导免疫抑制特性。Treg 细胞被认为是具有针对 T 效应细胞的强大抑制特性的主要免疫细胞亚群。然而,最近发现 Treg 细胞抑制中性粒细胞功能并促进其凋亡。Treg 细胞的作用机制之一是根据感染耐受模型诱导其他抑制细胞群。我们表明,LPS 激活的 Treg 细胞促进 IL-10 和 TGF-β1 的产生,抑制 PMN 产生 IL-6,并诱导血红素加氧酶-1 (HO-1) 和细胞因子信号转导抑制因子 3 分子 (SOCS3) 的表达。然而,CD3/CD28 激活的 Treg 细胞被发现可促进 TGF-β1 的产生,以及 PMN 中 IDO 和 HO-1 的表达。这些发现表明,Treg 细胞可能通过诱导具有免疫抑制特性的中性粒细胞产生 IL-10、TGF-β1、IDO 和 HO-1,在直接控制先天免疫反应中发挥重要作用。

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