ArticleInternational journal of women's health2025
Causal Effects of Inflammatory Cytokines and Immune Cell Phenotypes on Spontaneous Abortion: Evidence From Mendelian Randomization.
Article in International journal of women's health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Inflammatory factors and hypertensive nephropathy: A bidirectional 2-sample Mendelian randomization study.Medicine · 2026Article
- Evaluation of Neutrophil-to-Lymphocyte Ratio and Platelet-to-Lymphocyte Ratio as Biomarkers in Missed Abortions.Saudi medical journal · 2026Article
- C3a and TNF-α as potential biomarkers in recurrent spontaneous abortion: insights from integrated protein and gene expression analysis.Molecular biology reports · 2026Article
- Mendelian randomization reveals the associations between modifiable risk factors and intermediate phenotypes and spontaneous abortion.BMC pregnancy and childbirth · 2026Article
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Authors and funding
10 authors.
Funding
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Abstract
Purpose: This study aims to investigate the causal relationship between inflammatory cytokines, immune cells and spontaneous abortion (SA). Methods: A bidirectional two-sample Mendelian randomization (MR) analyses was conducted based on the genetic data of 91 inflammatory cytokines (n=14,824), 731 immune traits (n=3757) and SA (18,680 cases and 162,987 controls) cohorts. Five different MR analysis methods and Bayesian-weighted Mendelian randomization (BWMR) analysis were employed to assess the genetic causal connection. In addition, the robustness of this study results was ensured through comprehensive sensitivity analyses assessing heterogeneity, and potential horizontal pleiotropy and reverse causality. Results: These MR results suggest that higher levels of two inflammatory cytokines and ten immune cells are associated with a lower risk of SA (OR < 1.00). In contrast, fifteen immune cell traits exhibit a positive relationship with SA risk (OR > 1.00). Notably, mediation analysis revealed that the causal effect of programmed death ligand 1 (PDL1) on SA was partially mediated by CD45 expression on Granulocytic Myeloid-Derived Suppressor Cells (GR-MDSCs), and Terminally Differentiated CD4⁻CD8⁻ T cells also acted as mediators in the causal effect of tumor necrosis factor-beta (TNF-β) on SA. Conclusion: This study comprehensively assessed the causal relationship between immune-related exposures and SA, identifying several immune factors associated with SA risk. These finding have implications for clinical guidance in pregnancy preparation.
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