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Updated: May 5, 2026
Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
Published on: February 12, 2016
Causal relations between immune cells and cerebral hemorrhage: a bidirectional Mendelian randomization study
Zhimin Wu1, Qiqi Wang1, Zuojun Xiong1
1Department of Neurosurgery, The Central hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Insights
This study reveals a causal link between specific immune cells and intracerebral hemorrhage. Findings suggest immune cell changes may directly influence stroke development.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Previous research indicates a correlation between elevated immune cell counts and intracerebral hemorrhage (ICH).
- The precise causal link between immune cells and ICH remains unclear.
Purpose of the Study:
- To investigate the causal relationship between immune cells and intracerebral hemorrhage.
- Utilize a two-way Mendelian randomization (MR) approach.
Main Methods:
- Employed two sets of single nucleotide polymorphisms (SNPs) as instrumental variables.
- Conducted two-way MR analyses, including leave-one-out and MR-Egger tests.
- Performed meta-analysis to combine ICH datasets and assess heterogeneity.
Main Results:
- Identified a significant causal association between specific immune cells, including CD66b on Granulocytic Myeloid-Derived Suppressor Cells, and ICH.
- MR-Egger analysis indicated no significant genetic pleiotropy.
- Leave-one-out analysis confirmed the robustness of the MR results; no significant heterogeneity was detected.
Conclusions:
- Established a significant causal relationship between particular immune cell phenotypes and intracerebral hemorrhage.
- Mendelian randomization analysis provides strong evidence for immune cells influencing ICH.
Background:
Previous studies have shown that an increased number of immune cells is closely associated with the onset and course changes of intracerebral hemorrhage, but the exact causal relationship has not been clarified. The aim of this study was to investigate the causal relationship between immune cells and intracerebral hemorrhage by a two-way Mendelian randomization method.
Methods:
Two sets of SNPs were used as instrumental variables and two-way Mendelian randomization analyses were performed and leave-one-out method were used to assess the validity and heterogeneity of the included genetic variation instruments. The level of multiplicity and heterogeneity of the included genetic variance instruments was assessed.
Results:
The results showed a clear causal relationship between three immune cells and intracerebral hemorrhage, and no heterogeneity between SNPs related to intracerebral hemorrhage, while scatterplot and funnel plot confirmed that the causality was less likely to be biased; MR-Egger results suggested that no genetic pleiotropy was found. Leave-one-out analysis was applied to suggest that the MR analysis results for a single SNP were robust; meanwhile, Meta-analysis was applied to combine the two intracerebral hemorrhage datasets, and the analysis results suggested that in the fixed-effects model and random-effects model, the immunocyte CD66b on Granulocytic Myeloid-Derived Suppressor Cells and other three immune cells were significantly causally associated with intracerebral hemorrhage, while the heterogeneity test suggested that there was no significant difference between the different datasets.
Conclusions:
The present study found a significant causal relationship between specific immune cell phenotypes and intracerebral hemorrhage by Mendelian randomization analysis.
