ArticleBMC medicine2023
Dual-specificity phosphatases 22-deficient T cells contribute to the pathogenesis of ankylosing spondylitis.
Article in BMC medicine, 2023. 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, 12 citations in OpenAlex.
- DUSP family phosphatases in cell signaling, inflammation, and chronic diseases.Journal of biomedical science · 2026Review
- The dual-specificity phosphatase JSP1 regulates neutrophil adhesion via integrin-SRC signaling in vascular inflammation.The Journal of biological chemistry · 2026Article
- Dual-specificity phosphatase 14 inhibits the growth of cervical cancer cells by regulating the transforming growth factor-beta-activated kinase 1 and NOD-like receptor pyrin domain containing 3 inflammatory pathways.The Journal of international medical research · 2026Article
- Serum JKAP as a potential prognostic biomarker in acute coronary syndrome patients undergoing percutaneous coronary intervention.Frontiers in cardiovascular medicine · 2025Article
- Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025Review
- PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis.Cancer gene therapy · 2024Article
- miR-199a-5p targets DUSP14 to regulate cell proliferation, invasion and stemness in non-small cell lung cancer.Heliyon · 2024Article
- The phosphatase DUSP22 inhibits UBR2-mediated K63-ubiquitination and activation of Lck downstream of TCR signalling.Nature communications · 2024Article
- DNA methylation patterns in CD4Frontiers in immunology · 2023Article
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5 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundDual-specificity phosphatases (DUSPs) can dephosphorylate both tyrosine and serine/threonine residues of their substrates and regulate T cell-mediated immunity and autoimmunity. The aim of this study was to investigate the potential roles of DUSPs in ankylosing spondylitis (AS).
methodsSixty AS patients and 45 healthy controls were enrolled in this study. Associations of gene expression of 23 DUSPs in peripheral T cells with inflammatory cytokine gene expression and disease activity of AS were analyzed. Finally, we investigated whether the characteristics of AS are developed in DUSP-knockout mice.
resultsThe mRNA levels of DUSP4, DUSP5, DUSP6, DUSP7, and DUSP14 in peripheral T cells were significantly higher in AS group than those of healthy controls (all p < 0.05), while DUSP22 (also named JKAP) mRNA levels were significantly lower in AS group than healthy controls (p < 0.001). The mRNA levels of DUSP4, DUSP5, DUSP6, DUSP7, and DUSP14 in T cells were positively correlated with mRNA levels of tumor necrosis factor-α (TNF-α), whereas DUSP22 was inversely correlated (all p < 0.05). In addition, inverse correlations of DUSP22 gene expression in peripheral T cells with C-reactive protein, erythrocyte sedimentation rate, and Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) were observed (all p < 0.05). More importantly, aged DUSP22 knockout mice spontaneously developed syndesmophyte formation, which was accompanied by an increase of TNF-α
conclusionsDUSP22 may play a crucial role in the pathogenesis and regulation of disease activity of AS.
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