从类风湿性关节炎患者的Th17细胞中表达miR-146a及其与炎症性细胞因子的相关性

从类风湿性关节炎患者的Th17细胞中表达miR-146a及其与炎症性细胞因子的相关性

相关实验视频

Updated: Sep 20, 2025

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

381

Jinhui Tan¹, Linghua Tan², Hai Huang³

¹Department of Rheumatology and Immunology, People's Hospital of Longhua, Shenzhen, Guangdong 518109, PR China.

Immunobiology

|May 27, 2025

概括

微RNA-146a (miR-146a) 表达在类风湿性关节炎 (RA) T辅助细胞中升高,与炎症类细胞因子相关. 在RA患者中增加miR-146a水平降低了关键的炎症标志物,这表明治疗作用.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
类风湿病学类风湿病学

背景情况:

类风湿性关节炎 (RA) 是一种慢性自身免疫性疾病,其特征是关节炎症.
辅助性T细胞17 (Th17) 和相关的细胞因子在RA的发病过程中起着至关重要的作用.
微RNAs,如miR-146a在调节RA中的Th17细胞功能的作用尚未完全理解.

研究的目的:

在RA患者的外周血液Th17细胞中研究miR-146a的表达水平.
确定miR-146a表达和关键炎性细胞因子 (TNF-α,IL-6,IL-17) 在RA中的相关性.
探索调节miR-146a对RA Th17细胞中这些炎症标记物的功能影响.

主要方法:

定量实时PCR (qPCR) 用于测量miR-146a的表达.
流细胞计 (FCM) 用于量化TNF-α,IL-6和IL-17的水平.
在RA Th17细胞的体外转移与miR-146a模仿.
皮尔森相关性分析以评估miR-146a和细胞因子之间的关系.

主要成果:

与健康对照组相比,RA患者的Th17细胞中的miR-146a,TNF-α,IL-6和IL-17水平显著更高.
与miR-146a的传染模仿增加了miR-146a的表达,并在RA Th17细胞中显著降低了TNF-α,IL-6和IL-17水平.
在RA患者的miR-146a表达和TNF-α,IL-6和IL-17水平之间观察到正相关性,无论是在传染之前还是之后.

结论:

在RA患者的Th17细胞中,miR-146a的表达被上调.
调节Th17细胞中的miR-146a水平可以影响促炎细胞因子的分泌.
miR-146a可能通过影响Th17细胞的炎症性细胞因子产生在RA的发病过程中发挥作用.

关键词:

炎症性细胞因子类风湿性关节炎类风湿性关节炎类风湿性关节炎这是T淋巴细胞.在 miR-146a 里面.

更多相关视频

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

12:59

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

34.8K

Flow Cytometry Analysis of Immune Cell Subsets within the Murine Spleen, Bone Marrow, Lymph Nodes and Synovial Tissue in an Osteoarthritis Model

12:23

Flow Cytometry Analysis of Immune Cell Subsets within the Murine Spleen, Bone Marrow, Lymph Nodes and Synovial Tissue in an Osteoarthritis Model

Published on: April 24, 2020

20.0K

相关概念视频

01:24

T Cell Types and Functions

1.4K

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...

1.4K

01:20

The JAK-STAT Signaling Pathway

9.3K

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...