About
Titles
Assistant Professor
Biography
Dr. Tomokazu Sumida received his MD from Chiba University School of Medicine in Japan in 2004 and completed two years of residency, followed by two years of fellowship in cardiology. He practiced as a cardiologist in Japan before obtaining his PhD in 2012 studying the interface between the immune system and cardiovascular disease. To learn basic and translational immunology, he joined the lab of Dr. David Hafler at Yale in 2015 as a postdoctoral fellow. His research focus is mainly on understanding molecular mechanisms that drive T cell dysfunction, especially regulatory T cells, in human diseases by using cutting-edge technologies (i.e. Single-cell multi-omics, ATAC-seq, CRISPR gene editing/regulation). He was appointed as an assistant professor of neurology in 2020.
Appointments
Neurology
Assistant ProfessorPrimary
Other Departments & Organizations
- Hafler Lab
- Neurology
- Program for Neuroinflammation
Education & Training
- Instructor
- Yale School of Medicine (2020)
- Associate Research Scientist
- Yale School of Medicine (2019)
- Post doctoral Associate
- Yale School of Medicine (2017)
- Postdoctoral fellowship
- Yale School of Medicine (2016)
- PhD
- Chiba University, Graduate School of Medical and Pharmaceutical Sciences (2012)
- MD
- Chiba University, School of Medicine (2004)
Research
Overview
Medical Subject Headings (MeSH)
Autoimmune Diseases; Cardiovascular System; Immune System; Nervous System
ORCID
0000-0002-9806-2642- View Lab Website
Sumida Lab
Research at a Glance
Yale Co-Authors
Frequent collaborators of Tomokazu S Sumida's published research.
Publications Timeline
A big-picture view of Tomokazu S Sumida's research output by year.
Research Interests
Research topics Tomokazu S Sumida is interested in exploring.
David A. Hafler, MD, FANA
Naftali Kaminski, MD
Akiko Iwasaki, PhD
Jonas Christian Schupp, MD
Steven Kleinstein, PhD
Carrie L Lucas, PhD
37Publications
1,979Citations
Autoimmune Diseases
Publications
Featured Publications
Impaired TIGIT expression on B cells drives circulating follicular helper T cell expansion in multiple sclerosis
Asashima H, Axisa PP, Pham THG, Longbrake EE, Ruff WE, Lele N, Cohen I, Raddassi K, Sumida TS, Hafler DA. Impaired TIGIT expression on B cells drives circulating follicular helper T cell expansion in multiple sclerosis. Journal Of Clinical Investigation 2022, 132: e156254. PMID: 36250467, PMCID: PMC9566906, DOI: 10.1172/jci156254.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsRelapsing-remitting multiple sclerosisMemory B cellsCTfh cellsB cellsTIGIT expressionMultiple sclerosisT cellsFollicular helper T cellsHealthy age-matched controlsB-cell depletionT cell expansionHelper T cellsAge-matched controlsB cell functionB-cell pathwayDifferential gene expression signaturesTfh cellsDisease activityGene expression signaturesCell depletionCD40 ligandTranscription factor TCF4Disease pathogenesisImmune systemNew MRIA multiple sclerosis–protective coding variant reveals an essential role for HDAC7 in regulatory T cells
Axisa P, Yoshida T, Lucca L, Kasler H, Lincoln M, Pham G, Del Priore D, Carpier J, Lucas C, Verdin E, Sumida T, Hafler D. A multiple sclerosis–protective coding variant reveals an essential role for HDAC7 in regulatory T cells. Science Translational Medicine 2022, 14: eabl3651. PMID: 36516268, DOI: 10.1126/scitranslmed.abl3651.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsExperimental autoimmune encephalitisRegulatory T cellsHistone deacetylase 7Multiple sclerosisT cellsMouse modelFunction of Foxp3CD4 T cellsHigher suppressive capacityVivo modelingAutoimmune encephalitisEAE severityImmunosuppressive subsetAutoimmune diseasesImmunomodulatory roleSuppressive capacityImmune cellsDisease onsetDistinct molecular classesSusceptibility lociGenetic susceptibility lociSingle-cell RNA sequencingDisease riskPatient samplesProtective variantsIdentity thieves: T cells steal CD20 from B cells but mark themselves for certain death.
Sumida TS, O'Connor KC. Identity thieves: T cells steal CD20 from B cells but mark themselves for certain death. Science Immunology 2022, 7: eabq7242. PMID: 35522724, DOI: 10.1126/sciimmunol.abq7242.Peer-Reviewed Original ResearchCitationsAltmetricPopulation genetics meets single-cell sequencing
Sumida TS, Hafler DA. Population genetics meets single-cell sequencing. Science 2022, 376: 134-135. PMID: 35389792, DOI: 10.1126/science.abq0426.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsType I interferon transcriptional network regulates expression of coinhibitory receptors in human T cells
Sumida TS, Dulberg S, Schupp JC, Lincoln MR, Stillwell HA, Axisa PP, Comi M, Unterman A, Kaminski N, Madi A, Kuchroo VK, Hafler DA. Type I interferon transcriptional network regulates expression of coinhibitory receptors in human T cells. Nature Immunology 2022, 23: 632-642. PMID: 35301508, PMCID: PMC8989655, DOI: 10.1038/s41590-022-01152-y.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCoinhibitory receptor expressionHuman T cellsIFN-I responsesCoinhibitory receptorsT cellsTIGIT expressionReceptor expressionAcute SARS-CoV-2 infectionPD-1/TimSARS-CoV-2 infectionEnhancement of immunotherapyType 1 interferonT-cell featuresLAG-3Infectious diseasesDifferent temporal kineticsTranscription factorsCancer therapyReceptorsCell featuresKey transcription factorIFNPresent studyMRNA profilingKey regulatorSingle-cell multi-omics reveals dyssynchrony of the innate and adaptive immune system in progressive COVID-19
Unterman A, Sumida TS, Nouri N, Yan X, Zhao AY, Gasque V, Schupp JC, Asashima H, Liu Y, Cosme C, Deng W, Chen M, Raredon MSB, Hoehn KB, Wang G, Wang Z, DeIuliis G, Ravindra NG, Li N, Castaldi C, Wong P, Fournier J, Bermejo S, Sharma L, Casanovas-Massana A, Vogels CBF, Wyllie AL, Grubaugh ND, Melillo A, Meng H, Stein Y, Minasyan M, Mohanty S, Ruff WE, Cohen I, Raddassi K, Niklason L, Ko A, Montgomery R, Farhadian S, Iwasaki A, Shaw A, van Dijk D, Zhao H, Kleinstein S, Hafler D, Kaminski N, Dela Cruz C. Single-cell multi-omics reveals dyssynchrony of the innate and adaptive immune system in progressive COVID-19. Nature Communications 2022, 13: 440. PMID: 35064122, PMCID: PMC8782894, DOI: 10.1038/s41467-021-27716-4.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdaptive ImmunityAgedAntibodies, Monoclonal, HumanizedCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCells, CulturedCOVID-19COVID-19 Drug TreatmentFemaleGene Expression ProfilingGene Expression RegulationHumansImmunity, InnateMaleReceptors, Antigen, B-CellReceptors, Antigen, T-CellRNA-SeqSARS-CoV-2Single-Cell AnalysisConceptsProgressive COVID-19B cell clonesSingle-cell analysisT cellsImmune responseMulti-omics single-cell analysisCOVID-19Cell clonesAdaptive immune interactionsSevere COVID-19Dynamic immune responsesGene expressionSARS-CoV-2 virusAdaptive immune systemSomatic hypermutation frequenciesCellular effectsProtein markersEffector CD8Immune signaturesProgressive diseaseHypermutation frequencyProgressive courseClassical monocytesClonesImmune interactionsImmune dysregulation and autoreactivity correlate with disease severity in SARS-CoV-2-associated multisystem inflammatory syndrome in children
Ramaswamy A, Brodsky NN, Sumida TS, Comi M, Asashima H, Hoehn KB, Li N, Liu Y, Shah A, Ravindra NG, Bishai J, Khan A, Lau W, Sellers B, Bansal N, Guerrerio P, Unterman A, Habet V, Rice AJ, Catanzaro J, Chandnani H, Lopez M, Kaminski N, Dela Cruz CS, Tsang JS, Wang Z, Yan X, Kleinstein SH, van Dijk D, Pierce RW, Hafler DA, Lucas CL. Immune dysregulation and autoreactivity correlate with disease severity in SARS-CoV-2-associated multisystem inflammatory syndrome in children. Immunity 2021, 54: 1083-1095.e7. PMID: 33891889, PMCID: PMC8043654, DOI: 10.1016/j.immuni.2021.04.003.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMIS-C patientsDisease severityInflammatory syndromeTCR repertoireSARS-CoV-2-associated multisystem inflammatory syndromeAsymptomatic SARS-CoV-2 infectionSARS-CoV-2 infectionAdult COVID-19Post-infectious complicationsMultisystem inflammatory syndromeCytotoxicity genesHealthy pediatricImmune dysregulationMemory TActive infectionMyeloid dysfunctionPatientsSingle-cell RNA sequencingFlow cytometrySerum proteomicsRepertoire analysisElevated expressionSeverityAlarminsCOVID-19Cardiac dopamine D1 receptor triggers ventricular arrhythmia in chronic heart failure
Yamaguchi T, Sumida TS, Nomura S, Satoh M, Higo T, Ito M, Ko T, Fujita K, Sweet ME, Sanbe A, Yoshimi K, Manabe I, Sasaoka T, Taylor MRG, Toko H, Takimoto E, Naito AT, Komuro I. Cardiac dopamine D1 receptor triggers ventricular arrhythmia in chronic heart failure. Nature Communications 2020, 11: 4364. PMID: 32868781, PMCID: PMC7459304, DOI: 10.1038/s41467-020-18128-x.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsVentricular arrhythmiasDopamine D1 receptorsD1 receptorsChronic heart failureHeart failure patientsSustained ventricular tachycardiaNormal calcium handlingFailure patientsHeart failureModel miceVentricular tachycardiaPathophysiological roleCalcium handlingTherapeutic targetDopamine systemSingle-cell resolution analysisArrhythmiasD1RCardiomyocytesReceptorsTachycardiaPatientsMiceComplement C1q Activates Canonical Wnt Signaling and Promotes Aging-Related Phenotypes
Naito AT, Sumida T, Nomura S, Liu ML, Higo T, Nakagawa A, Okada K, Sakai T, Hashimoto A, Hara Y, Shimizu I, Zhu W, Toko H, Katada A, Akazawa H, Oka T, Lee JK, Minamino T, Nagai T, Walsh K, Kikuchi A, Matsumoto M, Botto M, Shiojima I, Komuro I. Complement C1q Activates Canonical Wnt Signaling and Promotes Aging-Related Phenotypes. Cell 2012, 149: 1298-1313. PMID: 22682250, PMCID: PMC3529917, DOI: 10.1016/j.cell.2012.03.047.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsComplement C1qWnt coreceptor low-density lipoprotein receptor-related protein 6Canonical Wnt signalingLow-density lipoprotein receptor-related protein 6Serum C1q concentrationLipoprotein receptor-related protein 6Age-related phenotypesWild-type miceAge-associated impairmentWnt signalingMuscle regenerationAge-associated declineYoung miceC1q treatmentC1q concentrationsSkeletal muscle regenerationMammalian agingMiceProtein 6C1qC1s inhibitionCanonical WntMultiple tissuesFrizzled receptorsWntComplement C1q-induced activation of β-catenin signalling causes hypertensive arterial remodelling
Sumida T, Naito AT, Nomura S, Nakagawa A, Higo T, Hashimoto A, Okada K, Sakai T, Ito M, Yamaguchi T, Oka T, Akazawa H, Lee JK, Minamino T, Offermanns S, Noda T, Botto M, Kobayashi Y, Morita H, Manabe I, Nagai T, Shiojima I, Komuro I. Complement C1q-induced activation of β-catenin signalling causes hypertensive arterial remodelling. Nature Communications 2015, 6: 6241. PMID: 25716000, PMCID: PMC4351572, DOI: 10.1038/ncomms7241.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsVascular smooth muscle cellsProliferation of VSMCsArterial remodellingΒ-catenin signalingΒ-cateninComplement C1qBlood pressure elevationEnd-organ damageNovel therapeutic targetSmooth muscle cellsMacrophage depletionImmune cellsPrecise molecular mechanismsTherapeutic targetStructural remodellingMuscle cellsRemodellingHypertensionArteriosclerosisComplement C1ActivationC1qMolecular mechanismsSignalingGene deletion
Academic Achievements & Community Involvement
honor Harry Weaver Scholar Awards
National AwardNMSSDetails07/01/2023United Statesactivity Interferons in Acute Viral Disease - Friend or Foe
Oral PresentationViral Infections & Inflammation Workshop 2022Details09/08/2022 - 09/09/2022Washington, DC, United Statesactivity Integrated Multi-Omics Profiling of Foxp3+ Regulatory T cells Identify Dysfunctional Program in Multiple Sclerosis
LectureCell Physiology SeminarDetails07/04/2022 - PresentTokyo, Tokyo, Japanhonor Race to Erase MS Young Investigator Award
National AwardRace to Erase MSDetails07/01/2020activity Dynamic gene regulatory network of IFN-beta response in human T cells
Poster PresentationFOCIS 2019Details06/18/2019 - 06/21/2019Boston, MA, United StatesCollaborators
News
News
- August 28, 2024Source: Yale News
Study Reveals Molecular Mechanism Behind MS and Other Autoimmune Diseases
- August 21, 2024
Unique Immune Profile Identified in Fibrotic Hypersensitivity Pneumonitis
- May 05, 2023Source: Stat News
What explains rare heart condition among young men after Covid vaccines? A new study offers clues
- February 27, 2022Source: Yale Daily News
Yale experts make strides in Multiple Sclerosis research