ArticleFrontiers in endocrinology2024
Causal role of immune cells in Hashimoto's thyroiditis: Mendelian randomization study.
Article in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Autoimmune thyroid disease and human health: a systematic review of Mendelian randomization studies.Frontiers in immunology · 2025Pooled it
- Biomarkers associated with Hashimoto's thyroiditis induced by viral infection: An integrative bioinformatics and machine learning.Journal of translational autoimmunity · 2026Article
- Exploring the functional role of palmitoylation genes in clear cell renal cell carcinoma and their impact on tumor microenvironment.BMC genomic data · 2026Article
- Unveiling the mediating role of immune cells in the link between pathogen infections and Hashimoto's thyroiditis.The Journal of international medical research · 2026Article
- Extracellular vesicles at the immune-metabolic crossroads of Hashimoto's thyroiditis and diabetes mellitus.Frontiers in immunology · 2026Review
- Hashimoto's thyroiditis: from pathogenesis to clinical management.Frontiers in endocrinology · 2026Review
- Sphingolipid Metabolism in the Pathogenesis of Hashimoto's Thyroiditis.International journal of molecular sciences · 2025Review
- Exploring the comorbidity mechanisms between atherosclerosis and hashimoto's thyroiditis based on microarray and single-cell sequencing analysis.Scientific reports · 2025Article
- Dysregulated tryptophan metabolism: driving T cell subsets and PI3K-Akt pathway alterations in Hashimoto's thyroiditis.Frontiers in immunology · 2025Article
- Mechanisms underlying the promotion of papillary thyroid carcinoma occurrence and progression by Hashimoto's thyroiditis.Frontiers in endocrinology · 2025Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Hashimoto's thyroiditis (HT) is a common autoimmune disease whose etiology involves a complex interplay between genetics and environment. Previous studies have demonstrated an association between immune cells and HT. However, the casual relationship was not clear. We aimed to explore the causal associations between signatures of immune cells and HT. Methods: In this study, bidirectional two-sample Mendelian randomization (MR) analysis was conducted to investigate the potential causal relationship between 731 immune cell signatures and HT by using genome-wide association study (GWAS) data. Heterogeneity and horizontal pleiotropy were detected through extensive sensitivity analyses. Results: The increased levels of six immune phenotypes were observed to be causally associated with increased risk of HT P < 0.01, which were CD3 on CM CD8br, CD3 on CD39+ secreting Treg, HLA DR on CD33dim HLA DR+ CD11b-, CD3 on CD4 Treg, CD62L- plasmacytoid DC %DC, and CD3 on CD45RA+ CD4+. In addition, the levels of FSC-A on HLA DR+ T cell and CD62L on monocyte were associated with disease risk of HT P < 0.01. In addition, HT also had causal effects on CD3 on CM CD8br, CCR2 on monocyte, CD25 on CD39+ resting Treg, and CCR2 on CD62L+ myeloid DC P < 0.05. Conclusions: In this study, we demonstrated the genetic connection between immune cell traits and HT, thereby providing guidance and direction for future treatment and clinical research.
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