Akiko Honobe‐Tabuchi

ORCID: 0009-0006-8649-847X
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About
Contact & Profiles
Research Areas
  • Cancer Immunotherapy and Biomarkers
  • Immune Cell Function and Interaction
  • Immunotherapy and Immune Responses
  • CAR-T cell therapy research
  • RNA Interference and Gene Delivery
  • Immune cells in cancer
  • Cytomegalovirus and herpesvirus research
  • Inflammatory Biomarkers in Disease Prognosis
  • Single-cell and spatial transcriptomics
  • Hepatitis B Virus Studies
  • Cancer Genomics and Diagnostics
  • Monoclonal and Polyclonal Antibodies Research
  • Autoimmune Bullous Skin Diseases
  • Ocular Diseases and Behçet’s Syndrome
  • Allergic Rhinitis and Sensitization
  • Dermatology and Skin Diseases
  • Food Allergy and Anaphylaxis Research
  • Mast cells and histamine
  • Pharmacogenetics and Drug Metabolism
  • T-cell and B-cell Immunology
  • Otitis Media and Relapsing Polychondritis
  • Infectious Diseases and Tuberculosis
  • Nanoplatforms for cancer theranostics
  • Cancer Treatment and Pharmacology
  • Urticaria and Related Conditions

University of Yamanashi
2021-2025

University of Yamanashi Hospital
2023

ABSTRACT Regulatory T (T reg ) cells have an immunosuppressive function, and programmed death‐1 (PD‐1)‐expressing reportedly induce resistance to PD‐1 blockade therapies through their reactivation. However, the effects of antigenicity on expression in therapy remain unclear. Here, we show that gain high antigen with antigenicity. Additionally, tumors for were resistant vivo due + ‐cell infiltration. Because such cytotoxic lymphocyte (CTLA)‐4 expression, could be overcome by combination...

10.1111/cas.70029 article EN cc-by-nc Cancer Science 2025-02-27

Some patients experience mixed response to immunotherapy, whose biological mechanisms and clinical impact have been obscure. We obtained two tumor samples from lymph node (LN) metastatic lesions in a same patient. Whole exome sequencing for the both tumors single-cell tumor-infiltrating lymphocytes (TIL) demonstrated significant difference clonality TILs' characteristics, especially exhausted T-cell clonotypes, although close relationship between cell clones were observed as of an overlapped...

10.1158/2767-9764.crc-22-0050 article EN cc-by Cancer Research Communications 2022-07-11

T-cell exhaustion is a major contributor to immunosuppression in the tumor microenvironment (TME). Blockade of key regulators exhaustion, such as programmed death 1, can reinvigorate tumor-specific T cells and activate antitumor immunity various types cancer. In this study, we identified that CD106 was specifically expressed exhausted CD8+ TME using single-cell RNA sequencing. High expression clinical samples corresponded improved response cancer immunotherapy. suppressed both vitro vivo,...

10.1158/0008-5472.can-23-0453 article EN Cancer Research 2024-04-18

<div>Abstract<p>T-cell exhaustion is a major contributor to immunosuppression in the tumor microenvironment (TME). Blockade of key regulators T-cell exhaustion, such as programmed death 1, can reinvigorate tumor-specific T cells and activate antitumor immunity various types cancer. In this study, we identified that CD106 was specifically expressed exhausted CD8<sup>+</sup> TME using single-cell RNA sequencing. High expression clinical samples corresponded improved...

10.1158/0008-5472.c.7311383 preprint EN 2024-07-02

<div>Abstract<p>T-cell exhaustion is a major contributor to immunosuppression in the tumor microenvironment (TME). Blockade of key regulators T-cell exhaustion, such as programmed death 1, can reinvigorate tumor-specific T cells and activate antitumor immunity various types cancer. In this study, we identified that CD106 was specifically expressed exhausted CD8<sup>+</sup> TME using single-cell RNA sequencing. High expression clinical samples corresponded improved...

10.1158/0008-5472.c.7311383.v1 preprint EN 2024-07-02
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