Kazuki Sato, PhD
Associate Research Scientist in Cell BiologyCards
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DNAM-1 promotes inflammation-driven tumor development via enhancing IFN-γ production
Nakamura-Shinya Y, Iguchi-Manaka A, Murata R, Sato K, Van Vo A, Kanemaru K, Shibuya A, Shibuya K. DNAM-1 promotes inflammation-driven tumor development via enhancing IFN-γ production. International Immunology 2021, 34: 149-157. PMID: 34672321, DOI: 10.1093/intimm/dxab099.Peer-Reviewed Original ResearchConceptsCD4+ T cellsDNAM-1T cellsTumor developmentIFN-gTumor cellsConventional CD4+ T cellsNatural killer (NK) cellsAccelerated growth of tumorsDNAM-1-deficient miceInteraction of DNAM-1CD8+ T cellsIFN-g productionChemical carcinogen 7,12-dimethylbenz[a]anthraceneIFN-g secretionGrowth of tumorsCarcinogen 7,12-dimethylbenz[a]anthraceneTumor immunityNK cellsActivating immunoreceptorTumorInflammatory conditionsUp-regulatedExpression levelsMiceDNAM-1 regulates Foxp3 expression in regulatory T cells by interfering with TIGIT under inflammatory conditions
Sato K, Yamashita-Kanemaru Y, Abe F, Murata R, Nakamura-Shinya Y, Kanemaru K, Muratani M, Veillette A, Goto M, Ito M, Shibuya A, Shibuya K. DNAM-1 regulates Foxp3 expression in regulatory T cells by interfering with TIGIT under inflammatory conditions. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2021309118. PMID: 34011606, PMCID: PMC8166105, DOI: 10.1073/pnas.2021309118.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsAntigens, Differentiation, T-LymphocyteForkhead Transcription FactorsGene Expression RegulationGraft vs Host DiseaseHumansImmune ToleranceMiceMice, Inbred BALB CMice, Inbred C57BLProtein BindingProto-Oncogene Proteins c-aktReceptors, ImmunologicReceptors, VirusSignal TransductionT Lineage-Specific Activation Antigen 1T-Lymphocytes, RegulatoryTOR Serine-Threonine KinasesWhole-Body IrradiationConceptsTreg cell functionDNAM-1TIGIT signalingTreg cellsFoxp3 expressionDevelopment of graft-versus-host diseaseCell functionMaintenance of Foxp3 expressionTransfer of Treg cellsWild-type Treg cellsGraft-versus-host diseaseInflammatory conditionsDNAM-1-deficientTreg cell dysfunctionRegulatory T cellsForkhead box P3Ligand CD155Treg functionImmune toleranceT cellsTIGITTregsInflammatory mediatorsInflammatory diseasesCell dysfunctionIntestinal Permeability and IgA Provoke Immune Vasculitis Linked to Cardiovascular Inflammation
Noval Rivas M, Wakita D, Franklin M, Carvalho T, Abolhesn A, Gomez A, Fishbein M, Chen S, Lehman T, Sato K, Shibuya A, Fasano A, Kiyono H, Abe M, Tatsumoto N, Yamashita M, Crother T, Shimada K, Arditi M. Intestinal Permeability and IgA Provoke Immune Vasculitis Linked to Cardiovascular Inflammation. Immunity 2019, 51: 508-521.e6. PMID: 31471109, PMCID: PMC6751009, DOI: 10.1016/j.immuni.2019.05.021.Peer-Reviewed Original ResearchConceptsKD vasculitisIntestinal permeabilityIntestinal barrier functionIL-1BMouse modelKawasaki diseaseIgA depositionPharmacological inhibitionPathogenesis of Kawasaki diseaseBarrier functionDevelopment of cardiovascular lesionsMucosal barrier dysfunctionVasculitis developmentIgA vasculitisCardiac inflammationKD patientsImmune vasculitisBarrier dysfunctionCardiovascular lesionsIgA nephropathySecretory immunoglobulin AGut permeabilityInterleukin-1bVasculitisElevated sIgAIdentification and isolation of splenic tissue-resident macrophage sub-populations by flow cytometry
Fujiyama S, Nakahashi-Oda C, Abe F, Wang Y, Sato K, Shibuya A. Identification and isolation of splenic tissue-resident macrophage sub-populations by flow cytometry. International Immunology 2018, 31: 51-56. PMID: 30256964, PMCID: PMC6364618, DOI: 10.1093/intimm/dxy064.Peer-Reviewed Original ResearchConceptsMarginal zone macrophagesMarginal zone metallophilic macrophagesMacrophage sub-populationsFlow cytometryMembrane antigen expressionTissue-resident macrophagesSub-populationsWhite pulp macrophagesAntigen expressionFunctional characterizationMetallophilic macrophagesTissue-specific environmentRed pulpMacrophagesIsolatesCutting Edge: Identification of Marginal Reticular Cells as Phagocytes of Apoptotic B Cells in Germinal Centers
Sato K, Honda S, Shibuya A, Shibuya K. Cutting Edge: Identification of Marginal Reticular Cells as Phagocytes of Apoptotic B Cells in Germinal Centers. The Journal Of Immunology 2018, 200: 3691-3696. PMID: 29686051, DOI: 10.4049/jimmunol.1701293.Peer-Reviewed Original ResearchImproved protocol for the isolation of naïve follicular dendritic cells
Sato K, Honda S, Shibuya A, Shibuya K. Improved protocol for the isolation of naïve follicular dendritic cells. Molecular Immunology 2016, 78: 140-145. PMID: 27639061, DOI: 10.1016/j.molimm.2016.09.011.Peer-Reviewed Original ResearchMarginal zone B cells exacerbate endotoxic shock via interleukin-6 secretion induced by Fcα/μR-coupled TLR4 signalling
Honda S, Sato K, Totsuka N, Fujiyama S, Fujimoto M, Miyake K, Nakahashi-Oda C, Tahara-Hanaoka S, Shibuya K, Shibuya A. Marginal zone B cells exacerbate endotoxic shock via interleukin-6 secretion induced by Fcα/μR-coupled TLR4 signalling. Nature Communications 2016, 7: 11498. PMID: 27146354, PMCID: PMC4858745, DOI: 10.1038/ncomms11498.Peer-Reviewed Original ResearchConceptsMZ B cellsToll-like receptor 4Systemic inflammatory responseB cellsInterleukin-6Interleukin-6 productionInflammatory responseEndotoxic shockIntravenous injectionMarginal zone B cellsToll-like receptor 4 signalingInflammatory response to lipopolysaccharideIntravenous injection of lipopolysaccharideWild-type miceInjection of lipopolysaccharidePro-inflammatory roleInterleukin-6 secretionPro-inflammatory cytokinesResponse to lipopolysaccharideBlood-borne pathogensMarginal zoneNF-kB signalingProlonged survivalMyD88 pathwayReceptor 4Increased CD11b+ Gr‐1+ cell population in the placenta after infection with Toxoplasma gondii
Takeshima K, Sato K, Nabekura T, Nagamune K, Hamada H, Yoshikawa H, Shibuya A, Shibuya K. Increased CD11b+ Gr‐1+ cell population in the placenta after infection with Toxoplasma gondii. Microbiology And Immunology 2015, 59: 95-98. PMID: 25557654, DOI: 10.1111/1348-0421.12225.Peer-Reviewed Original ResearchConceptsT. gondii infectionToxoplasma gondiiObligate intracellular protozoan pathogenMolecular mechanisms of immune responsesIntracellular protozoan pathogenImmune responsePhenotype of immune cellsFetal brain abnormalitiesProtozoan pathogensFeto-maternal interfaceCongenital toxoplasmosisMechanisms of immune responseToxoplasmaInnate immune responseImmune cellsMolecular mechanismsPlacentaFlow cytometryBrain abnormalitiesCell populationsInfectionGondiiToxoplasmosisPathogensCD11b(+Molecular characterization of the dimer formation of Fcα/μ receptor (CD351).
Takagaki K, Satoh K, Honda S, Shibuya A. Molecular characterization of the dimer formation of Fcα/μ receptor (CD351). Mol Immunol 2013, 56: 23-7. PMID: 23665380, DOI: 10.1016/j.molimm.2013.04.003.Peer-Reviewed Original Research
2026
Mast cell extracellular granules are bioactive condensates assembled by heparin and polyamine
Xiong Y, Tomares D, Guo J, Sato K, Zeng L, Tian Y, Su M, Albis A, Pant A, Pappu R, Su X. Mast cell extracellular granules are bioactive condensates assembled by heparin and polyamine. Nature Chemical Biology 2026, 1-12. PMID: 41760814, PMCID: PMC13010460, DOI: 10.1038/s41589-026-02165-6.Peer-Reviewed Original ResearchThis study investigates how mast cell extracellular granules form via interactions between heparin and polyamines, creating unique microenvironments that enhance immune mediator activity.
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