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Previously, a link between TNF\u03b1 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\u2019s 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, \u201c<jats:italic>ex vivo response<\/jats:italic>\u201d and clinical response to anti-TNF\u03b1 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 \u201c<jats:italic>ex vivo\u201d<\/jats:italic> 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.<\/jats:p>","DOI":"10.1038\/s41598-018-32485-0","type":"journal-article","created":{"date-parts":[[2018,9,13]],"date-time":"2018-09-13T09:56:26Z","timestamp":1536832586000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Genetic variant in IL-32 is associated with the ex vivo cytokine production of anti-TNF treated PBMCs from rheumatoid arthritis patients"],"prefix":"10.1038","volume":"8","author":[{"given":"Michelle S. M. 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