Takayuki Imanishi

ORCID: 0000-0003-1973-4277
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About
Contact & Profiles
Research Areas
  • Immune Response and Inflammation
  • Immune Cell Function and Interaction
  • interferon and immune responses
  • T-cell and B-cell Immunology
  • Inflammasome and immune disorders
  • Human-Automation Interaction and Safety
  • Birth, Development, and Health
  • Cell death mechanisms and regulation
  • Protein Tyrosine Phosphatases
  • Older Adults Driving Studies
  • Abdominal vascular conditions and treatments
  • NF-κB Signaling Pathways
  • Traffic and Road Safety

Kitasato University
2024

RIKEN Center for Integrative Medical Sciences
2007-2023

Kagawa University
2011

Nagoya University
2007

Japan Society for the Promotion of Science
2007

Abstract Toll-like receptors recognize pathogen-associated molecular patterns, activate innate immunity, and consequently modulate adaptive immunity in response to infections. TLRs are also expressed on T cells, it has been shown that cell activation is modulated by TLR ligands. However, the functions of Th1 Th2 effector cells mechanisms underlying TLR-mediated not fully understood. We analyzed downstream signaling events both cells. In mouse stimulation TLR2 but other directly induced IFN-γ...

10.4049/jimmunol.178.11.6715 article EN The Journal of Immunology 2007-06-01

Receptor-interacting protein kinase 1 (RIPK1) regulates cell death and inflammation. Here, we show that T cell-specific RIPK1 deficiency in mice leads to the premature senescence of cells induces various age-related diseases, resulting death. causes higher basal activation mTORC1 (mechanistic target rapamycin complex 1) drives enhanced cytokine production, induction senescence-related genes, increased caspase-3/7, which are restored by inhibition mTORC1. Critically, normal aged exhibit...

10.1126/sciadv.add6097 article EN cc-by-nc Science Advances 2023-01-25

Stimulator of interferon genes (STING) plays a key role in detecting cytosolic DNA and induces type I (IFN-I) responses for host defense against pathogens. Although T cells highly express STING, its physiological remains unknown. Here, we show that costimulation with the STING ligand cGAMP TCR leads to IFN-I production strongly inhibits T-cell growth. TCR-mediated mTORC1 activation sustained IRF3 are required cGAMP-induced production, activity is partially counteracted by cGAMP, thereby...

10.26508/lsa.201800282 article EN cc-by Life Science Alliance 2019-01-25

Effector, but not naïve, T cells are activated by toll-like receptor-2 (TLR2) stimulation, leading to cytokine production and proliferation. We found that the differential response is attributable lack of expression adaptor protein TIRAP in naive cells. induced upon T-cell receptor (TCR) stimulation sustained strong interleukin-2 (IL-2) signals. Expression requires TCR- IL-2-induced mTORC1 activation. TLR2 activation nuclear factor κB (NF-κB) ERK, much higher interferon-γ (IFN-γ) helper 1...

10.1016/j.celrep.2020.107911 article EN cc-by Cell Reports 2020-07-01
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