ArticleJCI insight2022
IL-4 prevents adenosine-mediated immunoregulation by inhibiting CD39 expression.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- CD39 on CD8European journal of immunology · 2026Review
- Bioinformatics analysis reveals shared gene signatures and molecular mechanisms between periodontitis and rheumatoid arthritis in the context of aging.Acta odontologica Scandinavica · 2026Article
- Restoring adenosine balance in axial spondyloarthritis: a stage-specific framework for immune and structural modulation.Frontiers in immunology · 2026Review
- CD73 Expression by CD4Immunology · 2025Article
- SNP rs10748643 determines CD39 expression in T and NK cells through altering NFIC binding affinity rather than interfering with RNA splicing.Frontiers in immunology · 2025Article
- The dichotomic role of cytokines in aging.Biogerontology · 2024Review
- CD39 Is Expressed on Functional Effector and Tissue-resident Memory CD8+ T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- CD200R activation on naïve T cells by B cells induces suppressive activity of T cells via IL-24.Cellular and molecular life sciences : CMLS · 2024Article
- T cell fate decisions during memory cell generation with aging.Seminars in immunology · 2023Review
- The interplay between the DNA damage response and ectonucleotidases modulates tumor response to therapy.Science immunology · 2023Review
- Circulating Ectonucleotidases Signal Impaired Myocardial Perfusion at Rest and Stress.Journal of the American Heart Association · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The ectonucleotidase CD39 functions as a checkpoint in purinergic signaling on effector T cells. By depleting eATP and initiating the generation of adenosine, it impairs memory cell development and contributes to T cell exhaustion, thereby causing defective tumor immunity and deficient T cell responses in older adults who have increased CD39 expression. Tuning enzymatic activity of CD39 and targeting the transcriptional regulation of ENTPD1 can be used to modulate purinergic signaling. Here, we describe that STAT6 phosphorylation downstream of IL-4 signaling represses CD39 expression on activated T cells by inducing a transcription factor network including GATA3, GFI1, and YY1. GATA3 suppresses ENTPD1 transcription through prevention of RUNX3 recruitment to the ENTPD1 promoter. Conversely, pharmacological STAT6 inhibition decreases T cell effector functions via increased CD39 expression, resulting in the defective signaling of P2X receptors by ATP and stimulation of A2A receptors by adenosine. Our studies suggest that inhibiting the STAT6 pathway to increase CD39 expression has the potential to treat autoimmune disease while stimulation of the pathway could improve T cell immunity.
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What OpenQuestion holds
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.