ArticlePLoS pathogens2011
HTLV-1 bZIP factor induces T-cell lymphoma and systemic inflammation in vivo.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers.
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Who cites it
199 citing papers in PubMed, 311 citations in OpenAlex.
- Integrated bioinformatics and feature selection-based discovery of ADP-ribosylation-associated biomarkers in non-small cell lung cancer.Oncology letters · 2026Article
- Rewiring of the Apoptotic Rheostat in HTLV-1 Infection and Adult T-Cell Leukemia/Lymphoma.Cancers · 2026Review
- Immunophenotype and proviral landscape of HTLV-1c infection and pulmonary disease.EBioMedicine · 2026Article
- HTLV-1 HBZ inhibits DHX9 to reprogram circRNA biogenesis in ATLL.Tumour virus research · 2026Article
- Immunological decoding of adult T cell leukemia - its cell of origin and oncogenesis.Biomarker research · 2026Review
- Review
- Transferrin Receptor Marks a Foxp3-Low Treg-like Inflammatory T Cell Subset Associated with Disease Severity in HAM/TSP.Pathogens (Basel, Switzerland) · 2026Article
- Viral-driven oncogenesis in T/NK-cell lymphomas: parallels and divergences between HTLV-1 and EBV.International journal of hematology · 2026Review
- Review
- Adult T-cell leukemia/lymphoma: molecular pathogenesis, emerging therapies, and future directions.Frontiers in oncology · 2026Review
- mGenes to cells : devoted to molecular & cellular mechanisms · 2025Article
- Article
- Viral oncogenes drive biphenotypic lymphoproliferative malignancy in transgenic mice.Scientific reports · 2025Article
- Bidirectional anti-tumor and immunological strategies by targeting GARP-TGF-β axis in adult T-cell leukemia/lymphoma.Leukemia · 2025Article
- Impact of HTLV-1 infection on clinicopathological characteristics and tumour immune microenvironment in colorectal cancer.Virchows Archiv : an international journal of pathology · 2025Article
- HTLV-1 and ATLL: Epidemiology, Oncogenesis, and Opportunities for Community-Informed Research in the United States.Viruses · 2025Review
- Untangling the causes of geographical disparities in the clinical outcome of HTLV-1 infection: a critical perspective on the contribution of viral genetic diversity.Journal of virology · 2025Review
- JunB-HBZ nuclear translocation by TGF-β is a key driver in HTLV-1-mediated leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Molecular mechanisms of viral oncogenesis in haematological malignancies: perspectives from metabolic reprogramming, epigenetic regulation and immune microenvironment remodeling.Experimental hematology & oncology · 2025Review
- Sustained inflammation during human T-lymphotropic virus type 1 infection: a wildfire contributing to disease progression.Frontiers in medicine · 2025Review
139 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Human T-cell leukemia virus type 1 (HTLV-1) is the causal agent of a neoplastic disease of CD4+ T cells, adult T-cell leukemia (ATL), and inflammatory diseases including HTLV-1 associated myelopathy/tropical spastic paraparesis, dermatitis, and inflammatory lung diseases. ATL cells, which constitutively express CD25, resemble CD25+CD4+ regulatory T cells (T(reg)). Approximately 60% of ATL cases indeed harbor leukemic cells that express FoxP3, a key transcription factor for T(reg) cells. HTLV-1 encodes an antisense transcript, HTLV-1 bZIP factor (HBZ), which is expressed in all ATL cases. In this study, we show that transgenic expression of HBZ in CD4+ T cells induced T-cell lymphomas and systemic inflammation in mice, resembling diseases observed in HTLV-1 infected individuals. In HBZ-transgenic mice, CD4+Foxp3+ T(reg) cells and effector/memory CD4+ T cells increased in vivo. As a mechanism of increased T(reg) cells, HBZ expression directly induced Foxp3 gene transcription in T cells. The increased CD4+Foxp3+ T(reg) cells in HBZ transgenic mice were functionally impaired while their proliferation was enhanced. HBZ could physically interact with Foxp3 and NFAT, thereby impairing the suppressive function of T(reg) cells. Thus, the expression of HBZ in CD4+ T cells is a key mechanism of HTLV-1-induced neoplastic and inflammatory 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.