氨基素/EGFR轴对控制自身免疫性糖尿病的贡献有限
Arielle Raugh1,2, Yi Jing3,2, Matthew L Bettini2
1Translational Biology and Molecular Medicine Graduate Program, Baylor College of Medicine, Houston, TX, 77030, USA.
Scientific reports
|October 31, 2023
概括
在1型糖尿病 (T1D) 中,调节性T细胞 (Tregs) 可能有组织修复的作用. 虽然Tregs产生安菲瑞古林,但这项研究发现它对NOD小鼠自身免疫糖尿病进展的影响有限.
科学领域:
- 免疫学 免疫学 免疫学
- 内分泌学 在内分泌学.
- 细胞生物学 细胞生物学
背景情况:
- 已知CD4+Foxp3+调节性T细胞 (Tregs) 在1型糖尿病 (T1D) 中具有免疫抑制作用.
- 新兴研究强调了Tregs的新型组织修复功能,包括皮生长因子受体 (EGFR) 的配体安菲瑞古林的产生.
- 在胰腺小岛恒温和自身免疫性糖尿病中Treg衍生的安菲瑞古林的作用仍然未确定.
研究的目的:
- 调查Tregs在T1D病变发生中的非免疫功能.
- 确定Tregs产生的安菲瑞古林是否促进岛屿组织的修复,并影响糖尿病的进展.
- 在自身免疫糖尿病的背景下,探索安菲瑞古林,EGFR和β细胞应激之间的相互作用.
主要方法:
- 在非肥胖糖尿病 (NOD) 小鼠中,通过透小岛的Tregs产生安菲瑞古林的分析.
- 对Tregs和胰腺β细胞上表达的表皮生长因子受体 (EGFR) 的评估.
- 对安菲瑞古林对β细胞内质网膜 (ER) 压力介质的直接作用的研究.
- 在缺乏安菲瑞古林的NOD小鼠中对自身免疫糖尿病进展的评估.
主要成果:
- 岛屿透的Tregs显示出对安菲瑞古林生产的增强能力.
- 发现Tregs和胰腺β细胞都能表达EGFR.
- 氨基氨基素被证明可以调节β细胞内ER压力的调解者.
- 缺乏安菲瑞古林的NOD小鼠没有表现出加速自发性自身免疫糖尿病.
结论:
- 虽然胰腺小岛中的Tregs可以产生安菲瑞古林并表达EGFR,而安菲瑞古林可以影响β细胞应激,但其在自身免疫糖尿病进展中的作用似乎有限.
- 这些发现表明,Treg介导的安菲瑞古林信号可能不是NOD小鼠模型中自身免疫糖尿病的主要驱动因素或抑制因素.
- 需要进一步的研究,以充分阐明Tregs在自身免疫性疾病期间维持组织平衡的复杂功能.
相关概念视频
Autoimmune Disorders
456
Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune...
Concept and Mechanism of Autoimmune Diseases
The immune...
456
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal
2.2K
Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
2.2K
Mitogens and the Cell Cycle
6.5K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.5K
Insulin: The Receptor and Signaling Pathways
1.2K
Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
1.2K
Glucagon-like Receptor Agonists
334
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
334
Hormones Regulating Blood Glucose
3.4K
Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
In addition to accelerating glucose uptake and utilization, insulin has...
3.4K


