Adult T cell leukemia/lymphoma (ATL) is an aggressive malignancy secondary to chronic infection with human T cell leukemia virus type 1 (HTLV-1). The viral oncoprotein Tax initiates T cell transformation through activation of critical cellular pathways, including NF-κB. Unexpectedly, Tax protein is not detectable in most ATL cells, in contrast to the HTLV-1 HBZ protein which antagonizes Tax effects. Here, we demonstrate that primary ATL cells from patients with acute or chronic ATL express very low levels of Tax mRNA and protein. Critically, survival of these primary ATL cells is dependent on continued Tax expression. Mechanistically, Tax extinction results in reversal of NF-κB activation, P53/PML activation and apoptosis. Tax drives interleukin-10 (IL-10) expression and recombinant IL-10 rescues the survival of tax-depleted primary ATL cells. These results demonstrate the critical role of continued Tax and IL-10 expression for the survival of primary ATL cells, highlighting their relevance as therapeutic targets.
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http://dx.doi.org/10.1038/s41408-023-00841-7 | DOI Listing |
Int Immunopharmacol
January 2025
Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Hubei Key Laboratory of Biological Targeted Therapy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, China; Hubei Engineering Research Center for Immunological Diagnosis and Therapy of Cardiovascular Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, China. Electronic address:
Background: Cardiac fibrosis, a critical factor in myocardial remodeling post-myocardial infarction (MI), can advance heart failure progression. Atractylenolide III (ATL-III), derived from Atractylodes lancea, has recognized antioxidant and anti-inflammatory effects; however, its influence on cardiac fibrosis remains unclear.
Methods: MI was induced in mice by permanent ligation of the left anterior descending (LAD) coronary artery, followed by 2 weeks of ATL-III or dimethyl sulfoxide (DMSO) treatment.
Expert Rev Hematol
December 2024
Department of Hematology, Osaka International Cancer Institute, Osaka, Japan.
Introduction: Spontaneous regression (SR) is observed in some patients with mature T-cell non-Hodgkin lymphoma (MTCL), including adult T-cell leukemia/lymphoma (ATL), although the incidence is rare.
Area Covered: We extracted 31 cases with MTCL who experienced SR based on a literature search and summarized the patient characteristics and clinical outcomes.
Expert Opinion: MTCL with SR included various subtypes, the most common being ATL ( = 17).
Leuk Res
December 2024
National Centre for Human Retrovirology and Department of Haematology, Imperial College Healthcare NHS Trust, UK; Department of Immunology & Inflammation, Imperial College London, UK. Electronic address:
Human T-cell leukaemia virus type-1 (HTLV-1) causes the highly aggressive malignancy adult T-cell leukaemia-lymphoma (ATL) in approximately 5 % of chronically infected carriers. HTLV-1 persists in the host by enhancing survival of infected-T-cells despite the presence of a strong immune response. Therefore, asymptomatic HTLV-1 carriers have a lifelong balance between infected cell proliferation and the host antiviral immune response.
View Article and Find Full Text PDFHeliyon
October 2024
Division of Tumor and Cellular Biochemistry, Department of Medical Sciences, University of Miyazaki, Kiyotake, Miyazaki, Japan.
Adult T-cell leukemia/lymphoma (ATLL) is a refractory blood cancer with severe immunodeficiency resulting from retroviral infection. ATLL develops in only 5 % of HTLV-1-infected individuals, but the entire mechanism of ATLL progression remains unknown. Since recent studies have reported that the gut microbiome influences the progression of various diseases, we hypothesized that ATLL is also related to the gut microbiome and aimed to investigate this relationship.
View Article and Find Full Text PDFVirol J
December 2024
Department of Microbiology, Kawasaki Medical School, Kurashiki, Okayama, Japan.
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