ArticlePLoS pathogens2022
EBV+ tumors exploit tumor cell-intrinsic and -extrinsic mechanisms to produce regulatory T cell-recruiting chemokines CCL17 and CCL22.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Epstein-Barr virus-driven immunosuppression in nasopharyngeal carcinoma: a comprehensive review of viral mechanisms, spatial tumor ecosystems, and precision therapeutics.Frontiers in immunology · 2026Pooled it
- The current role of immunotherapy in treating nasopharyngeal carcinoma.Human vaccines & immunotherapeutics · 2026Review
- B Cells and Tumor Immunometabolism: Emerging Insights into Immune Regulation and Therapeutic Resistance.Antibodies (Basel, Switzerland) · 2026Review
- HMGB1 Post-Translational Modifications in Epstein-Barr Virus-Associated Nasopharyngeal Carcinoma: Current Evidence, Emerging Mechanistic Concepts, and Unresolved Questions.International journal of molecular sciences · 2026Review
- EBV hijacks the metabolic function of CD73 to resist the antitumor function of NK cells.NPJ precision oncology · 2026Article
- Increased Expression of CXCL9, CXCL10, and CXCL11 in Epstein-Barr Virus-Associated Infectious Mononucleosis and the Role of CXCL5 as a Candidate Biomarker of Disease Severity.Pathogens (Basel, Switzerland) · 2026Article
- Research progress on the mechanisms of EB virus reshaping the immune microenvironment in nasopharyngeal carcinoma.Clinical and experimental medicine · 2026Review
- Molecular mechanisms of Epstein-Barr Virus in the pathogenesis of lymphomas and new opportunities for precision medicine.Discover oncology · 2026Review
- Identification of a Treg-related gene signature for predicting prognosis and immunosuppression in skin cutaneous melanoma.Clinical and experimental medicine · 2025Article
- Targeting fibroblast derived thrombospondin 2 disrupts an immune-exclusionary environment at the tumor front in colorectal cancer.Nature communications · 2025Article
- Macrophage fatty acid metabolism under chronic hypoxia shapes γδ T cell recruitment via CCL22.iScience · 2025Article
- Progress in structure-based drug development targeting chemokine receptors.Frontiers in pharmacology · 2025Review
- CCL17, CCL22 and their receptor CCR4 in hematologic malignancies.Discover oncology · 2024Review
- Manipulating host secreted protein gene expression: an indirect approach by HPV11/16 E6/E7 to suppress PBMC cytokine secretion.Virology journal · 2024Article
- A Narrative Review of the State of the Art of CCR4-Based Therapies in Cutaneous T-Cell Lymphomas: Focus on Mogamulizumab and Future Treatments.Antibodies (Basel, Switzerland) · 2024Review
- Aflatoxin B1 and Epstein-Barr virus-induced CCL22 expression stimulates B cell infection.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Downstream STING pathways IRF3 and NF-κB differentially regulate CCL22 in response to cytosolic dsDNA.Cancer gene therapy · 2024Article
- EBV and Lymphomagenesis.Cancers · 2023Review
- Mechanisms of T cell evasion by Epstein-Barr virus and implications for tumor survival.Frontiers in immunology · 2023Review
- FOXP3+ regulatory T cells and the immune escape in solid tumours.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Epstein-Barr Virus (EBV) is involved in the etiology of multiple hematologic and epithelial human cancers. EBV+ tumors employ multiple immune escape mechanisms, including the recruitment of immunosuppressive regulatory T cells (Treg). Here, we show some EBV+ tumor cells express high levels of the chemokines CCL17 and CCL22 both in vitro and in vivo and that this expression mirrors the expression levels of expression of the EBV LMP1 gene in vitro. Patient samples from lymphoblastic (Hodgkin lymphoma) and epithelial (nasopharyngeal carcinoma; NPC) EBV+ tumors revealed CCL17 and CCL22 expression of both tumor cell-intrinsic and -extrinsic origin, depending on tumor type. NPCs grown as mouse xenografts likewise showed both mechanisms of chemokine production. Single cell RNA-sequencing revealed in vivo tumor cell-intrinsic CCL17 and CCL22 expression combined with expression from infiltrating classical resident and migratory dendritic cells in a CT26 colon cancer mouse tumor engineered to express LMP1. These data suggest that EBV-driven tumors employ dual mechanisms for CCL17 and CCL22 production. Importantly, both in vitro and in vivo Treg migration was effectively blocked by a novel, small molecule antagonist of CCR4, CCR4-351. Antagonism of the CCR4 receptor may thus be an effective means of activating the immune response against a wide spectrum of EBV+ tumors.
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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.