Publications by authors named "Yorifumi Satou"

Article Synopsis
  • * It finds that the frequency of SIV-Gag-specific follicular CD8 T cells is linked to the amount of SIV-RNA, particularly in treated or naturally controlling macaques, while showing a different behavior in untreated macaques.
  • * The research indicates that the gene expression profile of fCD8 T cells in naturally controlled infections is more favorable compared to those under cART, suggesting that improving these cells may lead to potential curative strategies for HIV/SIV.
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Unlabelled: Enzootic bovine leukosis (EBL), although eradicated in some European countries, is still the most common neoplastic disease of cattle, caused by the bovine leukemia virus (BLV). During the progression of EBL, BLV-infected cells clonally expand, and some of which result in tumor onset. The clonality of BLV-infected cells is generally evaluated with NGS or Sanger sequencing.

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Background: T-SPOT.TB, one of the screening tests for latent tuberculosis infection (LTBI), yields invalid results in human T-cell leukemia virus type 1 (HTLV-1)-positive patients with rheumatoid arthritis. However, the detailed mechanisms behind this invalidation are unclear.

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3,3'-Diindolylmethane (DIM), a compound derived from natural fruits and vegetables, is widely recognized for its anti-cancer activity. However, its action mechanisms remain ambiguous. In this study, to study the molecular mechanism of 3,3'-Diindolylmethane, we identified a novel mutation in the gene of mitochondrial translation elongation factor EF-Ts (tsf1), a key factor in mitochondrial protein translation, that conferred DIM resistance to Schizosaccharomyces pombe.

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Cancer cells adeptly manipulate the tumor microenvironment (TME) to evade host antitumor immunity. However, the role of cancer cell-intrinsic signaling in shaping the immunosuppressive TME remains unclear. Here, we found that the Hippo pathway in cancer cells orchestrates the TME by influencing the composition of cancer-associated fibroblasts (CAFs).

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Article Synopsis
  • - HTLV-1 can quickly transform CD4+ T cells in a lab setting, but most infected people remain asymptomatic, indicating a balance between the virus and the host's immune response.
  • - The study found a variant in the HTLV-1 Tax301-309 viral antigen in individuals with a specific HLA-A24 type, which affected the detection of anti-Tax cytotoxic T cells (CTLs).
  • - More than half of the T-cell receptors (TCRs) from these anti-Tax CTLs failed to recognize the mismatched Tax301-309 peptides, underlining the need for precise matching of viral antigens in T-cell therapy for adult T-cell leukemia (ATL).
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Human immunodeficiency virus 1 (HIV-1) infection is characterized by a dynamic and persistent state of viral replication that overwhelms the host immune system in the absence of antiretroviral therapy (ART). The impact of prolonged treatment on the antiviral efficacy of HIV-1-specific CD8 T cells has nonetheless remained unknown. Here, we used single-cell technologies to address this issue in a cohort of aging individuals infected early during the pandemic and subsequently treated with continuous ART.

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The introduction of combined antiretroviral therapy (cART) has greatly improved the quality of life of human immunodeficiency virus type 1 (HIV-1)-infected individuals. Nonetheless, the ever-present desire to seek out a full remedy for HIV-1 infections makes the discovery of novel antiviral medication compelling. Owing to this, a new late-stage inhibitor, Lenacapavir/Sunlenca, an HIV multi-phase suppressor, was clinically authorized in 2022.

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Background: Highly transmissible viruses including SARS-CoV-2 frequently accumulate novel mutations that are detected via high-throughput sequencing. However, there is a need to develop an alternative rapid and non-expensive approach. Here we developed a novel multiplex DNA detection method Intelli-OVI for analysing existing and novel mutations of SARS-CoV-2.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has acquired multiple mutations since its emergence. Analyses of the SARS-CoV-2 genomes from infected patients exhibit a bias toward C-to-U mutations, which are suggested to be caused by the apolipoprotein B mRNA editing enzyme polypeptide-like 3 (APOBEC3, A3) cytosine deaminase proteins. However, the role of A3 enzymes in SARS-CoV-2 replication remains unclear.

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Despite extensive regulatory T cell (Treg) research, fundamental questions on dynamics remain to be answered. The current study aims to dissect several interwoven concepts in Treg biology, highlighting the 'self-reactivity' of Treg and their counterparts, namely naturally-arising memory-phenotype T-cells, as a key mechanism to be exploited by a human retroviral infection. We propose the novel key concept, , capturing self-reactivity in a quantifiable manner using the Nr4a3-Timer-of-cell-kinetics-and-activity (Tocky) technology.

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Article Synopsis
  • - The study focuses on understanding how HIV-1 latency is established and maintained, which is crucial for targeting the virus effectively.
  • - Researchers introduced a new model called HIV-Timer of cell kinetics and activity (HIV-Tocky) that uses dual fluorescence to track HIV provirus silencing and reactivation, allowing for a better analysis of latent HIV populations.
  • - The HIV-Tocky model distinguishes between two types of latent cells: those that are directly latent and those that have recently silenced, thereby enhancing our understanding of HIV reservoirs and potential treatment strategies to eliminate the virus.
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box O (FOXO) family proteins are expressed in various cells, and play crucial roles in cellular metabolism, apoptosis, and aging. FOXO1-null mice exhibit embryonic lethality due to impaired endothelial cell (EC) maturation and vascular remodeling. However, FOXO1-mediated genome-wide regulation in ECs remains unclear.

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The pandemic HIV-1, HIV-1 group M, emerged from a single spillover event of its ancestral lentivirus from a chimpanzee. During human-to-human spread worldwide, HIV-1 diversified into multiple subtypes. Here, our interdisciplinary investigation mainly sheds light on the evolutionary scenario of the viral budding system of HIV-1 subtype C (HIV-1C), a most successfully spread subtype.

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The gut microbiota has emerged as a key regulator of immune checkpoint inhibitor (ICI) efficacy. Therapeutic approaches aimed at manipulating the microbiota through targeted reconstitution to enhance cancer treatment outcomes have garnered considerable attention. A single live microbial biotherapeutic bacterium, MIYAIRI 588 strain (CBM588), has been shown to enhance the effects of ICI monotherapy in patients with advanced lung cancer.

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Human T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL). HTLV-1 carriers have a lifelong asymptomatic balance between infected cells and host antiviral immunity; however, 5-10% of carriers lose this balance and develop ATL. Coinfection with promotes ATL development, suggesting that the immunological status of infected individuals is a determinant of HTLV-1 pathogenicity.

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Article Synopsis
  • The text discusses the challenge of eliminating latent HIV-1 infected cells during treatment and highlights a lack of effective in vitro models for testing therapies.
  • It presents a new protocol for creating various types of HIV-infected Jurkat cells, including ones that produce the virus and those that are latent.
  • This protocol allows for testing antiviral agents and analyzing the HIV provirus, which helps improve HIV-1 treatment strategies and understand how different infected cells are selected over time.
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Viral cell-free DNA (cfDNA) in plasma has been widely evaluated for detecting cancer and monitoring disease in virus-associated tumors. We investigated whether the amount of cfDNA of human T-cell leukemia virus type 1 (HTLV-1) correlates with disease state in adult T-cell leukemia-lymphoma (ATL). HTLV-1 cfDNA in aggressive ATL was significantly higher than that in indolent ATL and asymptomatic carriers.

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Unlabelled: Excess stroma and cancer-associated fibroblasts (CAF) enhance cancer progression and facilitate immune evasion. Insights into the mechanisms by which the stroma manipulates the immune microenvironment could help improve cancer treatment. Here, we aimed to elucidate potential approaches for stromal reprogramming and improved cancer immunotherapy.

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Article Synopsis
  • Bovine leukemia virus (BLV) causes the growth of infected B lymphocytes and up to 5% of infected cows can develop enzootic bovine leukosis (EBL), which involves tumor cell proliferation.
  • Using viral integration site analysis through a DNA capture-sequencing method, researchers discovered that identical tumor clones can be found in both blood and tumor tissue, suggesting that these cancer cells can circulate within the bodies of EBL-infected cattle.
  • A new method called rapid amplification of integration sites (BLV-RAIS) was developed to efficiently diagnose EBL by detecting clonal expansion of BLV-infected cells, showing high diagnostic sensitivity and specificity, thus providing a reliable tool for early detection of EBL
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Human T-cell leukemia virus type 1 (HTLV-1), a retrovirus which mainly infects CD4 T cells and causes adult T-cell leukemia/lymphoma (ATL), is primarily transmitted direct cell-to-cell transmission. This feature generates a wide variety of infected clones in hosts, which are maintained clonal proliferation, resulting in the persistence and survival of the virus. The maintenance of the pool of infected cells is achieved by sculpting the immunophenotype of infected cells and modulating host immune responses to avoid immune surveillance.

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Regulatory T-cells (Treg) are considerably heterogeneous. Thymically derived Treg (tTreg) are those, which differentiate in the thymus, while peripherally derived Treg (pTreg) differentiate from peripheral mature CD4 T-cells. These two populations are often identified using markers such as neuropilin-1 and Helios (for tTreg) and ROR-γt (for pTreg) in intestines (Tanoue et al.

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Human T-cell leukemia virus type 1 (HTLV-1) is the causative infectious agent of adult T-cell leukemia/lymphoma (ATL) and chronic neurological disease. The disparity between silenced sense transcription versus constitutively active antisense (Hbz) transcription from the integrated provirus is not fully understood. The presence of an internal viral enhancer has recently been discovered in the Tax gene near the 3' long terminal repeat (LTR) of HTLV-1.

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Article Synopsis
  • Persistence of HIV-1 latent reservoir cells during antiretroviral therapy (ART) presents a significant challenge in curing HIV-1.
  • * Researchers developed the "widely distributed intact provirus elimination" (WIPE) assay, a long-term cell culture system that mimics the diverse infection scenarios of HIV-1.
  • * The WIPE assay allows for the evaluation of latency-reversing agents (LRAs) and demonstrates that combining LRAs with ART can effectively reactivate and help eliminate latent HIV-1 cells.
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