Evidence map›Paper›PMID 42183209›Full record

ArticleFrontiers in immunology2026

Smoking-induced HLA-DQA1 overexpression in T cells: a novel pathway in thyroid eye disease development.

Yuhe Su, Jiamin Cao

Abstract read
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Yuhe SuDepartment of Endocrinology, Xi'an No.3 Hospital, The Affiliated Hospital of Northwest University, Xi'an, Shaanxi, China.
Jiamin CaoDepartment of Ophthalmology, Third Xiangya Hospital, Central South University, Changsha, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Smoking is an established risk factor for thyroid eye disease (TED), its immunopathological mechanisms remain elusive. This study investigates how smoking exacerbates TED through immune cell dysregulation. Methods: National Health and Nutrition Examination Survey (NHANES) data (1999-2010; n = 62,160) was used to compare leukocyte profiles between smokers and non-smokers using non-parametric tests and meta-analysis, with validation using retrospective clinical data. TED was characterized by orbital immune infiltration via CIBERSORT in the GEO dataset GSE58331 (27 patients vs. 23 controls). Linear regression linked lymphocyte levels with thyroid hormones with validation using retrospective clinical data. Summary-data-based Mendelian randomization (SMR) analyzed causal relationships between blood-derived gene expression and TED risk. Smoking-induced transcriptomic changes were validated using GSE4806 (T cells from smokers vs non-smokers) and RT-qPCR. Results: Smokers exhibited decreased leukocytes and neutrophils but elevated lymphocytes (p<0.05). Lymphocyte percentages correlated positively with FT3 and TT3, The database findings were consistent with the clinical data results. Orbital tissues showed increased follicular helper T cells and plasma cells in TED patients. SMR confirmed HLA-DQA1 (β=0.76) and HLA-DQB1 (β=0.34) as causal TED risk factors (p-HEIDI>0.05). Smoking induced 406 upregulated genes (including HLA-DQA1/DQB1) and 31 downregulated genes in T cells. RT-qPCR confirmed that HLA-DQA1 expression was significantly upregulated in leukocytes from TED patients who smoke. Conclusion: Smoking exacerbates TED by elevating T cells and promoting HLA-DQA1 overexpression in peripheral T cells, provide a mechanistic justification for smoking cessation in TED management.

Indexed as

Graves OphthalmopathyHLA-DQ alpha-ChainsSmokingT-LymphocytesAdultFemaleHumansMaleMiddle AgedRetrospective StudiesHLA-DQA1 antigenHLA-DQ alpha-ChainsHLA-DQA1immune dysregulationlymphocytessmokingthyroid eye disease

Identifiers

PMID42183209
PMCPMC13192335

What Socratic holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.