相关实验视频

Updated: Jan 8, 2026

Inducing Apical Periodontitis in Mice

Inducing Apical Periodontitis in Mice

Published on: August 6, 2019

衰老的CD4+T细胞通过JAK-STAT-ROS-p38 MAPK驱动糖尿病牙周炎

M Zhang^1,2,3, L Meng^1,2,3, X Li^1,2,3

¹Department of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.

Journal of dental research

|December 17, 2025

概括

衰老的CD4+T细胞通过释放炎症因素和恶化骨质损失来驱动糖尿病牙周炎. 准这些细胞和相关途径为这种糖尿病并发症提供了新的治疗策略.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
牙周病学牙周病学

背景情况:

糖尿病牙周炎 (DPD) 是糖尿病的严重并发症,其特征是牙周组织迅速破坏.
CD4+ T 淋巴细胞在适应性免疫中至关重要,并通过免疫代谢失调参与DPD病变发生.
CD4+ T 细胞在 DPD 进展中的特定作用需要进一步研究.

研究的目的:

研究糖尿病牙周炎中CD4+T细胞的功能动态和病原性贡献.
阐明 CD4+ T 细胞介导的 DPD 病变发生过程中涉及的免疫代谢和信号通路.
为了确定缓解DPD进展的潜在治疗点.

主要方法:

来自DPD小鼠的牙组织的单细胞RNA测序.
使用DPD小鼠模型和收养转移实验进行实验确认.
信号通路的生物信息学分析 (JAK-STAT,p38 MAPK) 和通路活动和抑制的实验验证.

主要成果:

在DPD中发现了显著的CD4+T细胞衰老,实验证实并与加剧衰老相关分泌表型 (SASP) 释放有关.
衰老的CD4+T细胞促进自我放大的炎症循环,破坏Th17/Treg平衡并加剧骨质损失.
在DPD中,JAK-STAT和p38 MAPK通路被上调,它们的抑制降低了CD4+T细胞衰老. JAK-STAT的激活导致mtROS和TNF-α-p38 MAPK轴的激活,导致p53的上调和衰老.

结论:

衰老的CD4+T细胞通过SASP介导的炎症和免疫细胞招募在糖尿病牙周炎中发挥关键的病原作用.
在DPD中,JAK-STAT-mtROS和TNF-α-p38 MAPK信号通路是CD4+ T细胞衰老的关键媒介.
针对CD4+T细胞衰老和这些信号通路,为糖尿病牙周炎提供了一个有前途的治疗途径.

关键词:

收养转移收养转移细胞衰老细胞衰老免疫力是一种免疫力.这是一种炎症炎症炎症炎症.线粒体中的线粒体.氧化应激是一种氧化应激.

更多相关视频

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells

Published on: May 6, 2013

相关概念视频

The JAK-STAT Signaling Pathway

The JAK-STAT Signaling Pathway

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...

Pathophysiology of Diabetes

Pathophysiology of Diabetes

Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...

TGF - β Signaling Pathway

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...