ArticleFrontiers in endocrinology2019
Increased Human Interleukin-32 Expression Is Related to Disease Activity of Graves' Disease.
Article in Frontiers in endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Pathogenic genes associated with immune-related genes in graves' disease: a multi-omics Mendelian randomization analysis.Scientific reports · 2025Article
- Mini review: Interleukin-32 as a key mediator of type 1 diabetes pathogenesis.Frontiers in immunology · 2025Review
- STAT3 single-nucleotide variants in autoimmune thyroid disease in the Pakhtun population of Khyber Pakhtunkhwa, Pakistan.Gene reports · 2024Article
- Interleukin 32 participates in cardiomyocyte-induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway.Experimental and therapeutic medicine · 2022Article
- lncRNA:mRNA expression profile in CD4+ T cells from patients with Graves' disease.Endocrine connections · 2020Article
- Hemophilia A Inhibitor Subjects Show Unique PBMC Gene Expression Profiles That Include Up-Regulated Innate Immune Modulators.Frontiers in immunology · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, abnormal expression of interleukin-32 (IL-32) has been involved in various inflammatory or autoimmune diseases, but the level of IL-32 expression in Graves' disease (GD) is still unknown. This study is aimed to explore the human IL-32 expression in GD and the association of IL-32 expression with the disease activity of GD. A total of 125 GD patients and 97 normal controls (NC) were recruited in this study. We examined IL-32 mRNA level in peripheral blood mononuclear cells (PBMCs) of 43 GD patients and 41 controls using real-time polymerase chain reaction (RT-PCR). Serum IL-32 level of 40 GD patients and 34 controls was measured by enzyme linked immunosorbent assay (ELISA). In another cohort including 42 GD patients and 22 controls, we detected the percentages of IL-32α
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