ArticleThe Journal of experimental medicine2018
Signaling function of PRC2 is essential for TCR-driven T cell responses.
Article in The Journal of experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
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Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- CBX7 functions as a methylation-dependent inducer of gene transcription and regulator of cytosolic signaling in lymphoid cells.Science advances · 2026Article
- Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Clinical characteristics and molecular heterogeneity in Follicular lymphoma with extranodal involvement.Genome medicine · 2025Article
- Targeting EZH2 in autoimmune diseases: unraveling epigenetic regulation and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Treating human cancer by targeting EZH2.Genes & diseases · 2025Review
- EZH1/EZH2 inhibition enhances adoptive T cell immunotherapy against multiple cancer models.Cancer cell · 2025Article
- Polycomb repressive complex 2 (PRC2) pathway's role in cancer cell plasticity and drug resistance.Functional & integrative genomics · 2025Review
- EZH2 inhibition enhances T cell immunotherapies by inducing lymphoma immunogenicity and improving T cell function.Cancer cell · 2025Article
- Transient EZH2 Suppression by Tazemetostat during In Vitro Expansion Maintains T-Cell Stemness and Improves Adoptive T-Cell Therapy.Cancer immunology research · 2025Article
- PROTAC EZH2 degrader-1 overcomes the resistance of podophyllotoxin derivatives in refractory small cell lung cancer with leptomeningeal metastasis.BMC cancer · 2024Article
- Combination Therapies to Improve the Efficacy of Immunotherapy in Triple-negative Breast Cancer.Molecular cancer therapeutics · 2023Article
- Lsd1 safeguards T-cell development via suppressing endogenous retroelements and interferon responses.Life science alliance · 2023Article
- Bioinformatics-based analysis of potential candidates chromatin regulators for immune infiltration in osteoarthritis.BMC musculoskeletal disorders · 2022Article
- Review
- Regulation of CCL2 by EZH2 affects tumor-associated macrophages polarization and infiltration in breast cancer.Cell death & disease · 2022Article
- Link between the EZH2 noncanonical pathway and microtubule organization center polarization during early T lymphopoiesis.Scientific reports · 2022Article
- The Role of Oxidative Stress in Epigenetic Changes Underlying Autoimmunity.Antioxidants & redox signaling · 2022Review
- EZH2: Its regulation and roles in immune disturbance of SLE.Frontiers in pharmacology · 2022Review
- Review
- Temporal and Epigenetic Control of Plasticity and Fate Decision during CD8Cold Spring Harbor perspectives in biology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Differentiation and activation of T cells require the activity of numerous histone lysine methyltransferases (HMT) that control the transcriptional T cell output. One of the most potent regulators of T cell differentiation is the HMT Ezh2. Ezh2 is a key enzymatic component of polycomb repressive complex 2 (PRC2), which silences gene expression by histone H3 di/tri-methylation at lysine 27. Surprisingly, in many cell types, including T cells, Ezh2 is localized in both the nucleus and the cytosol. Here we show the presence of a nuclear-like PRC2 complex in T cell cytosol and demonstrate a role of cytosolic PRC2 in T cell antigen receptor (TCR)-mediated signaling. We show that short-term suppression of PRC2 precludes TCR-driven T cell activation in vitro. We also demonstrate that pharmacological inhibition of PRC2 in vivo greatly attenuates the severe T cell-driven autoimmunity caused by regulatory T cell depletion. Our data reveal cytoplasmic PRC2 is one of the most potent regulators of T cell activation and point toward the therapeutic potential of PRC2 inhibitors for the treatment of T cell-driven autoimmune diseases.
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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.