相关实验视频

Updated: Jun 30, 2025

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

通过IRF4介导的Treg表型切换可以加剧高氧诱导的膜上皮细胞损伤

He Langyue¹, Zhu Ying¹, Jiang Jianfeng¹

¹Department of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, China.

BMC pulmonary medicine

|March 16, 2024

概括

干扰素调节因子4 (IRF4) 通过促进调节性T细胞 (Treg) 切换,加剧支气管肺张症 (BPD) 中的肺损伤. 在小鼠模型中,IRF4淘汰会防止高氧诱导的BPD.

科学领域:

肺部医学肺部医学
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

支气管肺功能障碍症 (BPD) 涉及气囊管功能障碍症和炎症性肺部疾病.
干扰素调节因子4 (IRF4) 与炎症性肺部疾病有关,但其在BPD中的作用尚不清楚.

研究的目的:

研究IRF4在BPD病变发生过程中的作用和机制.
阐明IRF4如何影响T细胞调节 (Treg) 现型切换在过氧诱导的BPD中.

主要方法:

通过高氧暴露建立了BPD的小鼠模型.
使用ELISA,西式涂抹和流动细胞计量来分析肺组织标记物,包括IRF4,IL-17A,IL-6,SP-C,T1α,FOXP3+Tregs和FOXP3+RORγt+Tregs.
检查了IRF4淘汰赛小鼠,暴露于高氧,以评估IRF4的特定效应.

主要成果:

在BPD小鼠中,肺部结构有障碍,IRF4,IL-17A,IL-6和FOXP3+RORγt+Tregs增加,但SP-C,T1α和FOXP3+Tregs减少.
暴露于高氧的IRF4淘汰小鼠表现出肺部结构正常化,SP-C和T1α增加,IL-17A和IL-6减少,Treg群体向FOXP3+Tregs转移.
在过氧诱导的Treg表型切换中,IRF4起着至关重要的作用.

结论:

在高氧化下,IRF4介导的Treg表型切换会在BPD中加剧膜上皮细胞损伤.
向IRF4可能通过调节Treg反应和保护肺组织,为BPD提供治疗策略.

关键词:

支气管肺部发育不良症叉头转录因子3 叉头转录因子干扰素调节因子4 干扰素调节因子监管性T细胞监管性T细胞与网红酸相关的孤儿核受体与网红酸相关的孤儿核受体

更多相关视频

In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure

In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure

Published on: October 22, 2019

In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol

In Vitro Differentiation of Human CD4⁺FOXP3⁺ Induced Regulatory T Cells (iTregs) from Naïve CD4⁺ T Cells Using a TGF-β-containing Protocol

Published on: December 30, 2016

相关概念视频

T Cell Types and Functions

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation

Acute Respiratory Failure-II

Acute Respiratory Failure-II

Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include: