ArticleFrontiers in aging neuroscience2024
Exploration of the causal associations between circulating inflammatory proteins, immune cells, and neuromyelitis optica spectrum disorder: a bidirectional Mendelian randomization study and mediation analysis.
Article in Frontiers in aging neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Cerebrospinal Fluid Metabolites Mediate Immune Cell Effects on Chronic Pain.Molecular neurobiology · 2026Article
- Immune cells influence chronic spontaneous urticaria by inflammatory proteins: Mendelian randomization and bioinformatic analysis.The journal of allergy and clinical immunology. Global · 2026Article
- Causal Exposures of Immune Cells in Neuromyelitis Optica Spectrum Disorders: A Mendelian Randomization Study and Flow Cytometry Analysis.Brain and behavior · 2026Article
- The Causal Association between Plasma Metabolites-Mediated Immune Cells and Myocardial Infarction: A Mendelian Randomization Study.Arquivos brasileiros de cardiologia · 2026Article
- Circulating Inflammatory Proteins and Age-related Macular Degeneration: New Insights from Mendelian Randomization.Combinatorial chemistry & high throughput screening · 2026Article
- Observational and Genetic Association of Myelodysplastic Syndromes (MDS) and Autoimmune Diseases in Adults.Mediators of inflammation · 2026Article
- Decoding the triglyceride-glucose index in metabolic dysfunction-associated steatotic liver disease: integrative insights from Mendelian randomization, cross-tissue transcriptomics, and spatial multi-omics.International journal of surgery (London, England) · 2026Article
- Significant Interplay Between Lipids, Cytokines, Chemokines, Growth Factors, and Blood Cells in an Outpatient Cohort.International journal of molecular sciences · 2025Article
- Integrative multi-omics investigation of sleep apnea: gut microbiome metabolomics, proteomics and phenome-wide association study.Nutrition & metabolism · 2025Article
- The Role of Interleukin-24 and Downstream Pathways in Inflammatory and Autoimmune Diseases.Cell biochemistry and biophysics · 2025Review
- Exploring the effect of SGLT2 inhibitors on the risk of primary open-angle glaucoma using Mendelian randomization analysis.Scientific reports · 2025Article
- Integrating plasma proteomics and genome-wide association data to identify therapeutic targets for retinal neurodegenerative diseases in Europeans.International journal of ophthalmology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
Background: An increasing body of research has demonstrated a robust correlation between circulating inflammatory proteins and neuromyelitis optica spectrum disorders (NMOSD). However, whether this association is causal or whether immune cells act as mediators currently remains unclear. Methods: We employed bidirectional two-sample Mendelian randomization (TSMR) analysis to examine the potential causal association between circulating inflammatory proteins, immune cells, and NMOSD using data from genome-wide association studies (GWAS). Five different methods for Mendelian randomization analyses were applied, with the inverse variance-weighted (IVW) method being the primary approach. Sensitivity analyses were further performed to assess the presence of horizontal pleiotropy and heterogeneity in the results. Finally, a two-step Mendelian randomization (MR) design was employed to examine the potential mediating effects of immune cells. Results: A notable causal relationship was observed between three circulating inflammatory proteins (CSF-1, IL-24, and TNFRSF9) and genetically predicted NMOSD. Furthermore, two immune cell phenotypes, genetically predicted CD8 on naive CD8+ T cells, and Hematopoietic Stem Cell Absolute Count were negatively and positively associated with genetically predicted NMOSD, respectively, although they did not appear to function as mediators. Conclusion: Circulating inflammatory proteins and immune cells are causally associated with NMOSD. Immune cells do not appear to mediate the pathway linking circulating inflammatory proteins to NMOSD.
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