Related Experiment Video
Updated: May 17, 2025
05:10
Back Mechanical Sensitivity Assessment in the Rat for Mechanistic Investigation of Chronic Back Pain
Published on: August 30, 2022
2.6K
Genetically Supported Causality Between Immune Cells Traits and Low Back Pain: A Bi-Directional Two-Sample Mendelian
Jianbing Wang1,2, Mengye Zhu1,3, Yuhan Liu4
1Department of Pain Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People's Republic of China.
Journal of Pain Research
|March 31, 2025
Summary
This study found a genetic link between six immune cell types and low back pain (LBP) risk. These findings suggest immune cells may causally influence LBP development.
Area of Science:
- Immunology
- Genetics
- Pain Research
Background:
- Low back pain (LBP) is a prevalent condition with complex etiologies.
- Emerging evidence suggests a role for immune cells in LBP pathogenesis.
Purpose of the Study:
- To investigate the potential causal relationship between various immune cell types and the risk of developing LBP.
- To utilize a bi-directional Mendelian randomization (MR) approach to assess genetic predispositions.
Main Methods:
- Employed a bi-directional Mendelian randomization (MR) study design.
- Utilized Single Nucleotide Polymorphisms (SNPs) associated with immune cell abundance as instrumental variables.
- Applied the inverse variance weighted (IVW) method, with MR-Egger and MR-PRESSO for sensitivity analyses.
Main Results:
- Identified a significant causal association between six immune cell types and LBP risk (P < 0.05).
- Specific immune cell types, including CD4 Treg AC and CD19 on CD20-CD38-, showed a reduced risk of LBP.
- Reverse MR analysis indicated no significant causal effect of LBP on the investigated immune cell types.
Conclusions:
- Established a significant genetic link between specific immune cell populations and susceptibility to LBP.
- Findings support the role of immune dysregulation in LBP etiology.
- Provides a foundation for future research into targeted immunomodulatory therapies for LBP.
Related Concept Videos
01:29Autoimmune Disorders
348
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...
348
01:11Genome-wide Association Studies-GWAS
12.2K
Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
GWAS does not require the identification of the target gene involved in...
GWAS does not require the identification of the target gene involved in...
12.2K
01:24T Cell Types and Functions
689
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...
689
01:20The JAK-STAT Signaling Pathway
8.5K
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...
8.5K