Tsuneyasu Kaisho

ORCID: 0000-0003-2616-1665
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About
Contact & Profiles
Research Areas
  • Immune Response and Inflammation
  • Immunotherapy and Immune Responses
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • NF-κB Signaling Pathways
  • interferon and immune responses
  • Cancer Immunotherapy and Biomarkers
  • CAR-T cell therapy research
  • Immune cells in cancer
  • Cytokine Signaling Pathways and Interactions
  • Inflammasome and immune disorders
  • Cell Adhesion Molecules Research
  • Antimicrobial Peptides and Activities
  • Monoclonal and Polyclonal Antibodies Research
  • RNA Interference and Gene Delivery
  • Mast cells and histamine
  • Viral gastroenteritis research and epidemiology
  • Phagocytosis and Immune Regulation
  • IL-33, ST2, and ILC Pathways
  • Psoriasis: Treatment and Pathogenesis
  • Endoplasmic Reticulum Stress and Disease
  • Complement system in diseases
  • Glycosylation and Glycoproteins Research
  • Galectins and Cancer Biology
  • Pediatric health and respiratory diseases

Wakayama Medical University
2016-2025

RIKEN Center for Integrative Medical Sciences
2014-2025

Wakayama University
2022

Osaka University
2011-2020

Osaka International University
2011-2020

University of Minnesota
2001-2020

University of Colorado Denver
2020

Takeda (Japan)
2017

RIKEN
2003-2013

Oxford University Press (United Kingdom)
2012

Interferons (IFNs) are critical for protection from viral infection, but the pathways linking virus recognition to IFN induction remain poorly understood. Plasmacytoid dendritic cells produce vast amounts of IFN-α in response wild-type influenza virus. Here, we show that this requires endosomal genomic RNA and signaling by means Toll-like receptor 7 (TLR7) MyD88. Single-stranded (ssRNA) molecules nonviral origin also induce TLR7-dependent production inflammatory cytokines. These results...

10.1126/science.1093616 article EN Science 2004-02-24

Stimulation of Toll-like receptors (TLRs) triggers activation a common MyD88-dependent signaling pathway as well MyD88-independent that is unique to TLR3 and TLR4 pathways leading interferon (IFN)-β production. Here we disrupted the gene encoding Toll/IL-1 receptor (TIR) domain-containing adaptor, TRIF. TRIF-deficient mice were defective in both TLR3- TLR4-mediated expression IFN-β IRF-3. Furthermore, inflammatory cytokine production response ligand, but not other TLR ligands, was severely...

10.1126/science.1087262 article EN Science 2003-07-15

Abstract Stat3, a member of STAT, is activated by variety cytokines such as IL-6 family cytokines, granulocyte CSF, epidermal growth factor, and leptin. A recent study with mice genetically deficient in the Stat3 gene has revealed its important role early embryogenesis. To assess function adult tissues, we disrupted specifically T cells conditional targeting using Cre-loxP system. In Stat3-deficient cells, IL-6-induced proliferation was severely impaired. did not enhance cell cycle...

10.4049/jimmunol.161.9.4652 article EN The Journal of Immunology 1998-11-01

Viral infection and stimulation with lipopolysaccharide (LPS) or double stranded RNA (dsRNA) induce phosphorylation of interferon (IFN) regulatory factor (IRF)-3 its translocation to the nucleus, thereby leading IFN-β gene induction. Recently, two IκB kinase (IKK)–related kinases, inducible (IKK-i) TANK-binding 1 (TBK1), were suggested act as IRF-3 kinases be involved in production Toll-like receptor (TLR) signaling viral infection. In this work, we investigated physiological roles these by...

10.1084/jem.20040520 article EN The Journal of Experimental Medicine 2004-06-21

Abstract Toll‐like receptors (TLR) recognize microbial and viral patterns activate dendritic cells (DC). TLR distribution among human DC subsets is heterogeneous: plasmacytoid (PDC) express TLR1, 7 9, while other types do not TLR9 but TLR. Here, we report that mRNA for most expressed at similar levels by murine splenic sub‐types, including PDC, TLR3 preferentially CD8α + TLR5 TLR7 are selectively absent from the same subset. Consistent with latter, ligand activates – as measured survival ex...

10.1002/eji.200323797 article EN European Journal of Immunology 2003-03-07

Abstract LPS, a major component of the cell wall Gram-negative bacteria, can induce variety biological responses including cytokine production from macrophages, B proliferation, and endotoxin shock. All them were completely abolished in MyD88-deficient mice, indicating essential role MyD88 LPS signaling. However, cells still show activation NF-κB mitogen-activated protein kinase cascades, although significance this is not clear. In study, we have examined effects on dendritic (DCs) wild-type...

10.4049/jimmunol.166.9.5688 article EN The Journal of Immunology 2001-05-01

Dendritic cells (DCs) play a crucial role in the immune responses against infections by sensing microbial invasion through toll-like receptors (TLRs). In humans, two distinct DC subsets, CD11c− plasmacytoid DCs (PDCs) and CD11c+ myeloid (MDCs), have been identified can respond to different TLR ligands, depending on differential expression of cognate TLRs. this study, we examined effect TLR-7 ligands human subsets. Both subsets expressed could which enhanced survival upregulated surface...

10.1084/jem.20020207 article EN The Journal of Experimental Medicine 2002-05-28
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