ArticleEuropean journal of immunology2012
DUSP4 deficiency enhances CD25 expression and CD4+ T-cell proliferation without impeding T-cell development.
Article in European journal of immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Regulation of TCR signalling by tyrosine phosphatases: from immune homeostasis to autoimmunity.Immunology · 2012Pooled it
- The dual specificity phosphatase 2 act as distal regulatory node in T cell signaling.iScience · 2026Article
- DUSP4 promotes anti-tumor CD8Nature communications · 2026Article
- DUSP family phosphatases in cell signaling, inflammation, and chronic diseases.Journal of biomedical science · 2026Review
- INHBABMC cancer · 2025Article
- High-resolution profile of neoantigen-specific TCR activation links moderate stimulation to increased resilience of engineered TCR-T cells.Nature communications · 2024Article
- Expression profile of mRNAs and miRNAs related to mitogen-activated kinases in HaCaT cell culture treated with lipopolysaccharide a and adalimumab.Cell cycle (Georgetown, Tex.) · 2024Article
- Time-dependent cell-state selection identifies transiently expressed genes regulating ILC2 activation.Communications biology · 2023Article
- Exposure of volunteers to microgravity by dry immersion bed over 21 days results in gene expression changes and adaptation of T cells.Science advances · 2023Article
- STAT5b is a key effector of NRG-1/ERBB4-mediated myocardial growth.EMBO reports · 2023Article
- An integrative analysis of the single-cell transcriptome identifies DUSP4 as an exhaustion-associated gene in tumor-infiltrating CD8+ T cells.Functional & integrative genomics · 2023Article
- Dual-specificity phosphatases 22-deficient T cells contribute to the pathogenesis of ankylosing spondylitis.BMC medicine · 2023Article
- Combined Dusp4 and p53 loss with Dbf4 amplification drives tumorigenesis via cell cycle restriction and replication stress escape in breast cancer.Breast cancer research : BCR · 2022Article
- Evaluating the role of IDO1 macrophages in immunotherapy using scRNA-seq and bulk-seq in colorectal cancer.Frontiers in immunology · 2022Article
- Dual-Specificity Phosphatases and Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2022Review
- Developmental cell programs are co-opted in inflammatory skin disease.Science (New York, N.Y.) · 2021Article
- Single-cell transcriptome analysis of the heterogeneous effects of differential expression of tumor PD-L1 on responding TCR-T cells.Theranostics · 2021Article
- Article
- Generation of pralatrexate resistant T-cell lymphoma lines reveals two patterns of acquired drug resistance that is overcome with epigenetic modifiers.Genes, chromosomes & cancer · 2020Article
- Dynamic Roles for IL-2-STAT5 Signaling in Effector and Regulatory CD4Journal of immunology (Baltimore, Md. : 1950) · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
The differentiation and activation of T cells are critically modulated by MAP kinases, which are in turn feed-back regulated by dual-specificity phosphatases (DUSPs) to determine the duration and magnitude of MAP kinase activation. DUSP4 (also known as MKP2) is a MAP kinase-induced DUSP member that is dynamically expressed during thymocyte differentiation. We generated DUSP4-deficient mice to study the function of DUSP4 in T-cell development and activation. Our results show that thymocyte differentiation and activation-induced MAP kinase phosphorylation were comparable between DUSP4-deficient and WT mice. Interestingly, activated DUSP4(-/-) CD4(+) T cells were hyperproliferative while DUSP4(-/-) CD8(+) T cells proliferated normally. Further mechanistic studies suggested that the hyperproliferation of DUSP4(-/-) CD4(+) T cells resulted from enhanced CD25 expression and IL-2 signaling through increased STAT5 phosphorylation. Immunization of DUSP4(-/-) mice recapitulated the T-cell hyperproliferation phenotype in antigen recall responses, while the profile of Th1/Th2-polarized antibody production was not altered. Overall, these results suggest that other DUSPs may compensate for DUSP4 deficiency in T-cell development, MAP kinase regulation, and Th1/Th2-mediated antibody responses. More importantly, our data indicate that DUSP4 suppresses CD4(+) T-cell proliferation through novel regulations in STAT5 phosphorylation and IL-2 signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.