ArticleMedicine2019
Circulating JNK pathway-associated phosphatase level correlates with decreased risk, activity, inflammation level and reduced clinical response to tumor necrosis factor-α inhibitor in Crohn disease patients.
Article in Medicine, 2019. 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.
- Staphylococcus aureus regulates Th17 cells and autophagy via STING in chronic eosinophilic rhinosinusitis with nasal polyps.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2025Article
- Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025Review
- JNK pathway-associated phosphatase illustrates low expression and negative correlations with inflammation, disease activity, and T-helper 17 cells in inflammatory bowel disease children.Journal of clinical laboratory analysis · 2022Article
- Clinical value of serum JKAP in acute ischemic stroke patients.Journal of clinical laboratory analysis · 2022Article
- Dual specificity phosphatase 22 relates to skin lesion degree and biologics history, while its longitudinal elevation during treatment reflects better outcome in psoriasis patients.Journal of clinical laboratory analysis · 2022Article
- DNA Methylation of T Lymphocytes as a Therapeutic Target: Implications for Rheumatoid Arthritis Etiology.Frontiers in immunology · 2022Review
- Measurement of synovium and serum dual specificity phosphatase 22 level: Their inter-correlation and potency as biomarkers in rheumatoid arthritis.Journal of clinical laboratory analysis · 2022Article
- Reduced JKAP correlates with advanced disease features, inflammation, as well as increased exacerbation risk and severity in asthmatic children.Irish journal of medical science · 2021Article
- Longitudinal monitor of Jun N-terminal kinase pathway associated phosphatase reflects clinical efficacy to triple conventional disease-modifying anti-rheumatic drugs treatment in rheumatoid arthritis patients.Inflammopharmacology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to investigate the correlation of serum Jun-amino-terminal kinase (JNK) pathway-associated phosphatase (JKAP) level with disease risk, severity, inflammation, and treatment response to tumor necrosis factor (TNF)-α inhibitor in Crohn disease (CD) patients.
methodNinety-six active CD patients and 90 healthy controls (HCs) were consecutively enrolled. Serum JKAP level of participants was determined via enzyme-linked immunosorbent assay (ELISA). In CD patients, C-reactive protein (CRP), erythrocyte sedimentation rate, Crohn disease activity index (CDAI), and inflammatory cytokine levels (determined by ELISA) were recorded. All CD patients underwent infliximab (IFX) treatment for 12 weeks, then treatment response (defined as decrement of CDAI ≥70) was assessed at week 12 (W12).
resultsSerum JKAP level in CD patients was lower compared to HCs, and it disclosed a good predictive value for decreased CD risk; meanwhile, it was negatively correlated with CRP level, CDAI score, TNF-α, interleukin (IL)-6, and IL-17 levels in CD patients. Sixty-eight (70.8%) patients achieved treatment response to IFX at W12, and JKAP level was increased at W12 compared to baseline. Interestingly, baseline JKAP level in response patients was decreased compared to nonresponse patients, and it exhibited a good predictive value for decreased treatment response to IFX, multivariate logistic regression revealed that JKAP was an independent factor for predicting reduced IFX response.
conclusionCirculating JKAP expression correlates with decreased disease risk, activity, and inflammation level, and it could be served as a novel biomarker for predicting reduced clinical response to TNF-α inhibitor in CD patients.
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