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• W2891708682 abstract "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." @default.
• W2891708682 created "2018-09-27" @default.
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• W2891708682 date "2018-09-19" @default.
• W2891708682 modified "2023-10-10" @default.
• W2891708682 title "Genetic variant in IL-32 is associated with the ex vivo cytokine production of anti-TNF treated PBMCs from rheumatoid arthritis patients" @default.
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• W2891708682 doi "https://doi.org/10.1038/s41598-018-32485-0" @default.
• W2891708682 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6145899" @default.
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