Daniel Jane-Wit, MD/PhD
Associate Professor of Medicine (Cardiology) and ImmunobiologyDownloadHi-Res Photo
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Cardiovascular Medicine
Primary
Immunobiology
Secondary
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About
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Associate Professor of Medicine (Cardiology) and Immunobiology
Biography
I am a physician-scientist in the Section of Cardiovascular Medicine. My research laboratory studies the role of endothelial cells, the cells that line blood vessels, in solid organ transplant rejection. In this endeavor, we have developed novel, patient-centered protocols heavily incorporating human biospecimens to increase the likelihood that findings derived from these assays will be clinically relevant.
Appointments
Cardiovascular Medicine
Associate Professor on TermPrimaryImmunobiology
Associate Professor on TermSecondary
Other Departments & Organizations
- Cardiovascular Medicine
- Human and Translational Immunology Program
- Immunobiology
- Immunology
- Internal Medicine
- Vascular Biology and Therapeutics Program
- Yale Cardiovascular Research Center (YCVRC)
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
Education & Training
- Fellow
- Yale New Haven Hospital (2015)
- Resident
- Stanford Hospital and Clinics (2009)
- MD/PhD
- Case Western Reserve University School of Medicine (2006)
- BA
- Columbia University (1999)
Board Certifications
Nuclear Cardiology
- Certification Organization
- Certification Board of Nuclear Cardiology
- Original Certification Date
- 2016
Adult Echocardiography
- Certification Organization
- National Board of Echocardiography
- Original Certification Date
- 2015
Internal Medicine
- Certification Organization
- AB of Internal Medicine
- Latest Certification Date
- 2020
- Original Certification Date
- 2010
Research
Overview
Medical Research Interests
Endothelium, Vascular; Heart Transplantation; Transplantation Immunology
Research at a Glance
Yale Co-Authors
Frequent collaborators of Daniel Jane-Wit's published research.
Publications Timeline
A big-picture view of Daniel Jane-Wit's research output by year.
Research Interests
Research topics Daniel Jane-Wit is interested in exploring.
Jordan Pober, MD, PhD
Catherine Bingchan Xie, MD, PhD
George Tellides, MD, PhD
Clancy Mullan, MD, PhD
Francesc Lopez-Giraldez, PhD
Gilbert Moeckel, MD, PhD, FASN
8Publications
322Citations
Endothelium, Vascular
Publications
Featured Publications
ZFYVE21 is a complement-induced Rab5 effector that activates non-canonical NF-κB via phosphoinosotide remodeling of endosomes
Fang C, Manes TD, Liu L, Liu K, Qin L, Li G, Tobiasova Z, Kirkiles-Smith NC, Patel M, Merola J, Fu W, Liu R, Xie C, Tietjen GT, Nigrovic PA, Tellides G, Pober JS, Jane-wit D. ZFYVE21 is a complement-induced Rab5 effector that activates non-canonical NF-κB via phosphoinosotide remodeling of endosomes. Nature Communications 2019, 10: 2247. PMID: 31113953, PMCID: PMC6529429, DOI: 10.1038/s41467-019-10041-2.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAllograftsAnimalsCarrier ProteinsCell LineComplement Membrane Attack ComplexCoronary VesselsDisease Models, AnimalEndosomesFemaleGraft RejectionHuman Umbilical Vein Endothelial CellsHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsMiceMice, SCIDNF-kappa BPhosphatidylinositol PhosphatesRab5 GTP-Binding ProteinsUbiquitin-Protein LigasesVasculitisConceptsNF-κB-inducing kinaseMembrane attack complexNon-canonical NF-κBNF-κBEC activationEndothelial cellsTransplant organ rejectionConnective tissue diseaseHumanized mouse modelAllograft vasculopathySynovial tissueTissue diseaseVascular inflammationOrgan rejectionPharmacologic alterationsMouse modelDependent mannerAttack complexProteasome-dependent degradationInductionEndothelial Cell–Derived Interleukin-18 Released During Ischemia Reperfusion Injury Selectively Expands T Peripheral Helper Cells to Promote Alloantibody Production
Liu L, Fang C, Fu W, Jiang B, Li G, Qin L, Rosenbluth J, Gong G, Xie CB, Yoo P, Tellides G, Pober JS, Jane-Wit D. Endothelial Cell–Derived Interleukin-18 Released During Ischemia Reperfusion Injury Selectively Expands T Peripheral Helper Cells to Promote Alloantibody Production. Circulation 2019, 141: 464-478. PMID: 31744330, PMCID: PMC7035199, DOI: 10.1161/circulationaha.119.042501.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsDelayed Graft FunctionFemaleGene Expression RegulationHuman Umbilical Vein Endothelial CellsHumansImmunoglobulin MInflammasomesInterleukin-18Interleukin-18 Receptor alpha SubunitIsoantibodiesMiceMice, SCIDOrgan TransplantationReperfusion InjurySignal TransductionT-Lymphocytes, Helper-InducerConceptsIschemia-reperfusion injuryDonor-specific antibodiesPeripheral helper cellsIL-18Helper cellsReperfusion injuryInterleukin-18IL-18R1Donor-specific antibody formationEndothelial cellsDelayed graft functionLate allograft lossT cell populationsAlloantibody productionAllograft lossChronic rejectionGraft functionClinical manifestationsPD-L2Antibody formationHumanized modelAllograft tissueImmunoglobulin MPatient specimensComplement activationAlloantibody and Complement Promote T Cell–Mediated Cardiac Allograft Vasculopathy Through Noncanonical Nuclear Factor-&kgr;B Signaling in Endothelial Cells
Jane-wit D, Manes TD, Yi T, Qin L, Clark P, Kirkiles-Smith NC, Abrahimi P, Devalliere J, Moeckel G, Kulkarni S, Tellides G, Pober JS. Alloantibody and Complement Promote T Cell–Mediated Cardiac Allograft Vasculopathy Through Noncanonical Nuclear Factor-&kgr;B Signaling in Endothelial Cells. Circulation 2013, 128: 2504-2516. PMID: 24045046, PMCID: PMC3885874, DOI: 10.1161/circulationaha.113.002972.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCardiac allograft vasculopathyPanel reactive antibodyNuclear factor-κB signalingFactor-κB signalingAllograft vasculopathyT cellsEndothelial cellsMembrane attack complexAlloreactive T cell activationChronic antibody-mediated rejectionNoncanonical nuclear factorProinflammatory gene programAntibody-mediated rejectionDonor-specific antibodiesGraft endothelial cellsLate allograft lossAlloreactive T cellsAllogeneic endothelial cellsT cell activationAttack complexHuman T cellsAllograft lossHeart transplantationTransplantation patientsLesion pathogenesisComplement membrane attack complexes activate noncanonical NF-κB by forming an Akt+NIK+ signalosome on Rab5+ endosomes
Jane-wit D, Surovtseva YV, Qin L, Li G, Liu R, Clark P, Manes TD, Wang C, Kashgarian M, Kirkiles-Smith NC, Tellides G, Pober JS. Complement membrane attack complexes activate noncanonical NF-κB by forming an Akt+NIK+ signalosome on Rab5+ endosomes. Proceedings Of The National Academy Of Sciences Of The United States Of America 2015, 112: 9686-9691. PMID: 26195760, PMCID: PMC4534258, DOI: 10.1073/pnas.1503535112.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsBaculoviral IAP Repeat-Containing 3 ProteinClathrinComplement Membrane Attack ComplexCoronary VesselsEndocytosisEndosomesEnzyme StabilityFlow CytometryHuman Umbilical Vein Endothelial CellsHumansHydrazonesInhibitor of Apoptosis ProteinsMice, SCIDNF-kappa BProtein BiosynthesisProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktRab5 GTP-Binding ProteinsRNA, Small InterferingSecretory VesiclesSignal TransductionTNF Receptor-Associated Factor 3Ubiquitin-Protein LigasesConceptsNF-κB-inducing kinaseMembrane attack complexNoncanonical NF-κBGenome-wide siRNA screenComplement membrane attack complexNIK stabilizationDynamin-dependent mannerNoncanonical NF-κB signalingEndothelial cellsActive Rab5Attack complexSiRNA screenNF-κBAkt activationCytokine-mediated activationNF-κB signalingIκB kinaseSignalosomeRab5EndosomesKinaseAktInternalizationCoronary endothelial cellsActivationComplement Membrane Attack Complexes Assemble NLRP3 Inflammasomes Triggering IL-1 Activation of IFN-γ–Primed Human Endothelium
Xie CB, Qin L, Li G, Fang C, Kirkiles-Smith NC, Tellides G, Pober JS, Jane-Wit D. Complement Membrane Attack Complexes Assemble NLRP3 Inflammasomes Triggering IL-1 Activation of IFN-γ–Primed Human Endothelium. Circulation Research 2019, 124: 1747-1759. PMID: 31170059, PMCID: PMC6557295, DOI: 10.1161/circresaha.119.314845.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMembrane attack complexEndothelial cellsComplement membrane attack complexIL-1βNLRP3 inflammasomeEC immunogenicityComplement activationAntibody-mediated complement activationInflammasome assemblyComplement-mediated pathologiesRenal allograft biopsiesGraft endothelial cellsHuman coronary artery graftsLate allograft failureCoronary artery graftsT cell responsesImmune-mediated pathologyActivate endothelial cellsIL-1 receptorIL-1 synthesisIL-1β secretionNoncanonical NF-κB signalingNF-κB signalingAttack complexImmunodeficient mouse hostsA ZFYVE21-Rubicon-RNF34 signaling complex promotes endosome-associated inflammasome activity in endothelial cells
Li X, Jiang Q, Song G, Barkestani M, Wang Q, Wang S, Fan M, Fang C, Jiang B, Johnson J, Geirsson A, Tellides G, Pober J, Jane-wit D. A ZFYVE21-Rubicon-RNF34 signaling complex promotes endosome-associated inflammasome activity in endothelial cells. Nature Communications 2023, 14: 3002. PMID: 37225719, PMCID: PMC10209169, DOI: 10.1038/s41467-023-38684-2.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsEndothelial cellsInflammasome activityMembrane attack complexCaspase-1Potential therapeutic targetChronic rejectionComplement membrane attack complexTissue inflammationNLRP3 inflammasomeTissue injuryMouse modelTherapeutic targetDependent mannerInflammationAttack complexInflammasomeHuman tissuesFlightless IInhibitory associationsSkin modelRNF34CellsHedgehog-induced ZFYVE21 promotes chronic vascular inflammation by activating NLRP3 inflammasomes in T cells
Jiang B, Wang S, Song G, Jiang Q, Fan M, Fang C, Li X, Soh C, Manes T, Cheru N, Qin L, Ren P, Jortner B, Wang Q, Quaranta E, Yoo P, Geirsson A, Davis R, Tellides G, Pober J, Jane-Wit D. Hedgehog-induced ZFYVE21 promotes chronic vascular inflammation by activating NLRP3 inflammasomes in T cells. Science Signaling 2023, 16: eabo3406. PMID: 36943921, PMCID: PMC10061549, DOI: 10.1126/scisignal.abo3406.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsIschemia-reperfusion injuryChronic vascular inflammationT cellsNLRP3 inflammasomeVascular inflammationChronic inflammationEndothelial cellsIFN-γ responsesControl T cellsNLRP3 inflammasome activityT memory cellsAllograft vasculopathyVascular sequelaeHuman endothelial cellsCoronary arteryEffector responsesCell-autonomous roleInflammasome activityMouse modelInflammationPatient samplesVigorous recruitmentInflammasomePrimary human cellsImmune signaling
2024
IL-1β Induces Human Endothelial Surface Expression of IL-15 by Relieving let-7c-3p Suppression of Protein Translation.
Mullan C, Summer L, Lopez-Giraldez F, Tobiasova Z, Manes T, Yasothan S, Song G, Jane-Wit D, Saltzman W, Pober J. IL-1β Induces Human Endothelial Surface Expression of IL-15 by Relieving let-7c-3p Suppression of Protein Translation. The Journal Of Immunology 2024, 213: 1338-1348. PMID: 39302113, PMCID: PMC11493510, DOI: 10.4049/jimmunol.2400331.Peer-Reviewed Original ResearchConceptsIL-15Surface expressionIL-1BIL-15 transcriptsEndothelial cellsCD8 T cell activationExpression of IL-15EC surface expressionIL-15 transpresentationComplement activationGraft endothelial cellsActivity of CTLT cell activationIL-15 mRNAEndothelial surface expressionAbsence of complement activationCultured human endothelial cellsIL-1-mediated activationIL-15RAProtein translationAllograft rejectionRNA polymerase II-mediated transcriptionHuman endothelial cellsSuppression of protein translation
Academic Achievements & Community Involvement
activity Member, Thesis Committee, Dept of Immunobiology
CommitteesMemberDetailsThesis committee member for Abeer Obaid, a PhD candidate.2021 - 2022activity International Society of Heart and Lung Transplantation
Professional OrganizationsMemberDetails2018 - 2021activity American Society of Transplantation
Professional OrganizationsMemberDetails2018 - 2021activity Federation of Clinical Immunology Societies
Meeting Planning and ParticipationMemberDetails2017 - 2021activity American Heart Association
Meeting Planning and ParticipationMemberDetails2016 - 2021
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