ArticleScientific reports2018
Genetic variant in IL-32 is associated with the ex vivo cytokine production of anti-TNF treated PBMCs from rheumatoid arthritis patients.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Spatial transcriptomics identifies IL-32 as a lipid droplet-associated cytokine linked to tubular injury in human diabetic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Integrating multi-omic QTLs and predictive models reveals regulatory architectures at immune related GWAS loci in CD4+ T cells.medRxiv : the preprint server for health sciences · 2026Article
- Mini review: Interleukin-32 as a key mediator of type 1 diabetes pathogenesis.Frontiers in immunology · 2025Review
- Estimation of Interleukin 32 and Interleukin 37 Serum Levels in Iraqi Patients with Rheumatoid Arthritis.Archives of Razi Institute · 2023Article
- Biomarkers (mRNAs and non-coding RNAs) for the diagnosis and prognosis of rheumatoid arthritis.Frontiers in immunology · 2023Review
- A Critical Overview of Interleukin 32 in Leishmaniases.Frontiers in immunology · 2022Review
- Effects of IL-32 polymorphisms and IL-32 levels on the susceptibility and severity of coronary artery disease.Journal of clinical laboratory analysis · 2022Article
- Review
- Inhibition of IL-32 Expression Ameliorates Cerebral Ischemia-Reperfusion Injury via the NOD/MAPK/NF-κB Signaling Pathway.Journal of molecular neuroscience : MN · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
About 60% of RA patients don't achieve good response with biological disease-modifying anti-rheumatic drugs bDMARD treatment (including TNF inhibitors, TNFi's). Previously, a link between TNFα and interleukin (IL)-32 was reported in RA. However, the exact mechanism linking IL-32 to response to treatment as not been studied yet. Therefore, we explored the influence of a promoter single nucleotide polymorphism (SNP) rs4786370 in IL-32 on clinical responsiveness to TNFi's in RA patients, potentially serving as new biomarker in RA. Expression of pro-inflammatory cytokines by peripheral mononuclear cells (PBMCs) from RA patients and healthy individuals were studied. Moreover, "ex vivo response" and clinical response to anti-TNFα therapy (etanercept, adalimumab) were measured and stratified for the IL-32 SNP. Higher IL-32 protein production was observed in RA patients. Additionally, patients bearing the CC genotype showed higher IL-32 protein and cytokine expression. DAS28 was independent of the promoter SNP, however, the "ex vivo" cytokine response was not. IL-32 mRNA and protein production was higher in RA patients, with a trend towards higher concentrations in patients bearing the CC genotype. Furthermore, genotype dependent IL-1 beta production might predict clinical response to etanercept/adalimumab. This indicates that IL-32 could play a role in predicting response to treatment in RA.
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