通过增加炎症性细胞因子,Th17细胞和纤维化,SARS-CoV-2尖端蛋白加速系统性硬化
Ha Yeon Jeong1,2,3, Jin-Sil Park1,2, Jin Seok Woo1,2
1The Rheumatism Research Center, Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, Seoul, 06591, Korea.
Journal of inflammation (London, England)
|December 22, 2023
概括
SARS-CoV-2 尖端蛋白可能通过增加纤维化,炎症,自身抗体产生和血栓形成来恶化系统性硬化 (SSc). 这项研究探讨了COVID-19和SSc进展之间的联系.
科学领域:
- 免疫学 免疫学 免疫学
- 类风湿病学 类风湿病学
- 病毒学 病毒学
背景情况:
- 冠状病毒疾病2019 (COVID-19) 与系统性硬化症 (SSc) 等自身免疫性疾病共享症状.
- 尽管有一份病例报告表明存在联系,但COVID-19对SSc的确切影响仍然不清楚.
研究的目的:
- 研究SARS-CoV-2尖端蛋白对系统性硬化症 (SSc) 的影响.
- 阐明COVID-19可能影响SSc发展和进展的机制.
主要方法:
- 在hEK293细胞中纤维化标志物的体外分析感染了SARS-CoV-2尖端蛋白.
- 在体内研究,使用暴露于SARS-CoV-2尖端蛋白和ACE2受体的布莱米辛诱导的SSc小鼠模型.
- 纤维化,自身抗体,血栓性因素和炎症性细胞因子的评估.
主要成果:
- 在体外增加纤维化标志物;增加皮肤厚度和SSc小鼠纤维化暴露于尖端蛋白.
- 观察到自身抗体 (包括抗脂抗体) 和血栓性因素的显著增加.
- 在SSc小鼠中,对促炎性细胞因子IL-17的升调和恶化的组织纤维化和炎症.
结论:
- COVID-19可能通过加剧纤维化加速SSc.
- 这种加速可能是由炎症增加,自身抗体产生和血栓形成的媒介.
- 似乎SARS-CoV-2尖端蛋白在加剧SSc病理方面发挥着关键作用.
相关概念视频
01:20The JAK-STAT Signaling Pathway
8.9K
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...
8.9K
01:24T Cell Types and Functions
1.0K
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...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
1.0K
01:03Rous Sarcoma Virus (RSV) and Cancer
5.1K
Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
5.1K
02:26NF-κB-dependent Signaling Pathway
7.4K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
NF-κB-dependent Signaling Mechanism
The...
7.4K
01:05Single Nucleotide Polymorphisms-SNPs
15.1K
A single nucleotide polymorphism or SNP is a single nucleotide variation at a specific genomic position in a large population. It is the most prevalent type of sequence variation found in the human genome. Point mutations that occur in more than 1% of the population qualify as SNPs. These are present once every 1000 nucleotides on an average in the human genome. Replacement of a purine with another purine (A/G) or a pyrimidine with another pyrimidine (C/T) is known as a transition. In contrast,...
15.1K