相关实验视频

Updated: Sep 17, 2025

Quantification of Atherosclerosis in Mice

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

在C-C化学受体4缺乏症加剧小鼠早期动脉样硬化

Toru Tanaka¹, Naoto Sasaki^1,2, Aga Krisnanda¹

¹Laboratory of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Japan.

|July 3, 2025

概括

在小鼠中,C-C化学受体4 (CCR4) 的遗传缺失加速了动脉样硬化. 这与调节性T细胞功能受损和炎症增加有关,这表明CCR4对这种心血管疾病有负面调节作用.

科学领域:

免疫学免疫学免疫学
心血管疾病研究研究
分子生物学分子生物学

背景情况:

慢性炎症和T细胞失调是动脉样硬化心血管疾病发病的关键.
平衡促炎性T细胞和调节性T细胞 (Tregs) 是动脉样硬化的一种潜在的治疗策略.
已知C-C化学受体4 (CCR4) 在T细胞招募到炎症组织中的作用,但其在动脉样硬化中的特定功能尚不清楚.

研究的目的:

研究CCR4在早期动脉样硬化病变的发展中的作用.
阐明CCR4在动脉样硬化背景下影响T细胞反应的机制.

主要方法:

使用过高胆固醇的小鼠模型,基因删除了CCR4.
分析了早期动脉样硬化病变的发展和斑块表型.
评估了各种组织中的T辅助型1 (Th1) 细胞反应,包括外周淋巴体器官,准大动脉淋巴结和大动脉.
研究了CCR4缺乏对Treg抑制功能和迁移的影响.
在CCR4介导的免疫反应的背景下,研究了树突细胞功能的调节.

主要成果:

基因删除CCR4加速了具有炎症表型的早期动脉样硬化病变的发展.
在多种组织中,CCR4缺乏导致增强的前炎性Th1细胞反应.
在Tregs中CCR4缺乏会损害它们的抑制功能和迁移到大动脉.
这导致通过缺陷的树突细胞调节增强了Th1细胞介导的免疫反应,加速了大动脉炎症和病变的发展.

结论:

在控制动脉样硬化的早期阶段中,CCR4起着至关重要的,以前未知的作用.
CCR4通过Treg-依赖的T细胞反应的调节来调节动脉样硬化.
CCR4作为动脉样硬化的重要负调节剂,突出其作为治疗点的潜力.

关键词:

一个T细胞细胞.动脉样硬化动脉样硬化化学因子受体的化学因子受体免疫学免疫学免疫学这是一种炎症炎症炎症炎症.医学医学医学医学医学这里是鼠标鼠标鼠标鼠标鼠标鼠标.

更多相关视频

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Published on: December 7, 2013

相关概念视频

Atherosclerosis I: Introduction

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...

Inflammation

Inflammation

Coronary Artery Disease I: Introduction

Coronary Artery Disease I: Introduction

Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...