Featured Publications
Hyperosmotic stress response regulates interstitial homeostasis and pathogenic inflammation
Sumida T. Hyperosmotic stress response regulates interstitial homeostasis and pathogenic inflammation. The Journal Of Biochemistry 2023, 173: 159-166. PMID: 36722164, DOI: 10.1093/jb/mvad009.Peer-Reviewed Original ResearchConceptsHyperosmotic stress responseStress responseCell type-specific mannerFundamental cellular responsesType-specific mannerHeat shock proteinsCell cycle arrestImmune cell differentiationOsmolyte synthesisContext of diseaseHyperosmotic stressIon transportersHyperosmotic responseMetabolic remodelingMolecular mechanismsCellular responsesShock proteinsCell differentiationHuman diseasesCellular shrinkageCycle arrestAdaptative responseSpecific mannerTissue microenvironmentTissue immune homeostasisActivated β-catenin in Foxp3+ regulatory T cells links inflammatory environments to autoimmunity
Sumida T, Lincoln MR, Ukeje CM, Rodriguez DM, Akazawa H, Noda T, Naito AT, Komuro I, Dominguez-Villar M, Hafler DA. Activated β-catenin in Foxp3+ regulatory T cells links inflammatory environments to autoimmunity. Nature Immunology 2018, 19: 1391-1402. PMID: 30374130, PMCID: PMC6240373, DOI: 10.1038/s41590-018-0236-6.Peer-Reviewed Original ResearchConceptsProstaglandin E receptor 2Regulatory T cellsTreg cellsT cellsAnti-inflammatory cytokine productionIL-10 productionPeripheral immune toleranceIL-10 expressionΒ-cateninE receptor 2Treg subpopulationsTreg phenotypeIL-10Cytokines IFNImmune toleranceTreg signatureCytokine signatureMultiple sclerosisAutoimmune diseasesCytokine productionInflammatory environmentLethal autoimmunityReceptor 2Activated β-cateninIFN
2021
Tet2 Controls the Responses of β cells to Inflammation in Autoimmune Diabetes
Rui J, Deng S, Perdigoto AL, Ponath G, Kursawe R, Lawlor N, Sumida T, Levine-Ritterman M, Stitzel ML, Pitt D, Lu J, Herold KC. Tet2 Controls the Responses of β cells to Inflammation in Autoimmune Diabetes. Nature Communications 2021, 12: 5074. PMID: 34417463, PMCID: PMC8379260, DOI: 10.1038/s41467-021-25367-z.Peer-Reviewed Original ResearchConceptsImmune cellsΒ-cellsNOD/SCID recipientsDiabetogenic immune cellsDiabetogenic T cellsBone marrow transplantType 1 diabetesExpression of TET2Human β-cellsIslet infiltratesSCID recipientsMarrow transplantInflammatory pathwaysTransfer of diseaseT cellsInflammatory genesImmune killingPathologic interactionsReduced expressionDiabetesInflammationTET2MiceRecipientsCells
2017
DNA single-strand break-induced DNA damage response causes heart failure
Higo T, Naito AT, Sumida T, Shibamoto M, Okada K, Nomura S, Nakagawa A, Yamaguchi T, Sakai T, Hashimoto A, Kuramoto Y, Ito M, Hikoso S, Akazawa H, Lee JK, Shiojima I, McKinnon PJ, Sakata Y, Komuro I. DNA single-strand break-induced DNA damage response causes heart failure. Nature Communications 2017, 8: 15104. PMID: 28436431, PMCID: PMC5413978, DOI: 10.1038/ncomms15104.Peer-Reviewed Original ResearchConceptsPressure overload-induced heart failureOverload-induced heart failureHeart failureSingle-strand breaksNF-κB signalingNew therapeutic strategiesSSB accumulationDDR activationInflammatory cytokinesTherapeutic strategiesUnrepaired single-strand breaksDNA damageDNA single-strand breaksCausative roleDNA damage responseGenetic deletionPathogenesisActivationPivotal roleFailureDamage responseHeartCritical roleCytokinesMice