Clara Abraham, MD
Professor of Medicine (Digestive Diseases)Cards
Appointments
Digestive Diseases
Primary
Contact Info
Yale School of Medicine
Department of Medicine (Digestive Diseases), PO Box 208019
New Haven, CT 06520-8019
United States
About
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Titles
Professor of Medicine (Digestive Diseases)
Appointments
Digestive Diseases
ProfessorPrimary
Other Departments & Organizations
Education & Training
- MD
- University of Chicago Pritzker School of Medicine (1989)
- BS
- University of Illinois at Urbana-Champaign (1985)
Research
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Overview
Medical Research Interests
Colitis, Ulcerative; Crohn Disease; Genetics; Immune System; Immunity, Innate; Inflammation; Inflammatory Bowel Diseases; Intestines; Molecular Biology; T-Lymphocytes
ORCID
0000-0002-6435-0451
Research at a Glance
Yale Co-Authors
Frequent collaborators of Clara Abraham's published research.
Publications Timeline
A big-picture view of Clara Abraham's research output by year.
Research Interests
Research topics Clara Abraham is interested in exploring.
Kishu Ranjan, PhD
Badr Al Bawardy, MD
Carlos Fernandez-Hernando, PhD
Craig Roy, PhD
David A. Hafler, MD, FANA, MSc
Harriet Kluger, MD
26Publications
8,898Citations
Inflammatory Bowel Diseases
Intestines
Crohn Disease
Immunity, Innate
Colitis, Ulcerative
T-Lymphocytes
Publications
2025
Autophagy and Bacterial infections
Cadwell K, Abraham C, Bel S, Chauhan S, Coers J, Colombo M, Davis J, Hofius D, Nguyen H, Ogawa M, Roy C, Shao F, Shizukuishi S, Stallings C, Szczesna M, Taylor G, Thurston T, Watson R, Wileman T, Xu Y, Zamboni D. Autophagy and Bacterial infections. Autophagy Reports 2025, 4: 2542904. PMID: 40910070, PMCID: PMC12407897, DOI: 10.1080/27694127.2025.2542904.Peer-Reviewed Original ResearchCitationsConceptsLC3-associated phagocytosisBacterial effector proteinsEffector-triggered immunityMolecular mechanismsDouble-membrane autophagosomesEffective antimicrobial responsesEffector proteinsGene linksAutophagic membranesBacterial handlingAntimicrobial responsesIntracellular pathogensAutophagy initiationAntimicrobial defensePathogen clearancePathogensInflammatory defenseXenophagyAutophagySingle membraneBacterial infectionsAutophagy inhibitionDefenseTherapeutic potentialMembraneRoles of endothelial cells during infection
Ma Z, Pierce R, Lucas C, Abraham C, Fernandez-Hernando C, Jane-Wit D. Roles of endothelial cells during infection. Current Opinion In Immunology 2025, 97: 102648. PMID: 40885094, PMCID: PMC12433145, DOI: 10.1016/j.coi.2025.102648.Peer-Reviewed Original ResearchCitationsAltmetricConceptsEndothelial cellsChronic formVascular roleVaso-occlusive lesionsChronic vascular infectionBlood endothelial cellsChronic form of infectionClinical benefitOrgan dysfunctionVascular malformationsElectrolyte disturbancesSeptic shockAcute infectionVascular infectionsBarrier breakdownVascular functionMaladaptive inflammationTherapeutic implicationsHost defenseTissue pathologyVascular quiescenceInfectionPathologyCellsMalformations
2023
ScRNA-seq defines dynamic T-cell subsets in longitudinal colon and peripheral blood samples in immune checkpoint inhibitor-induced colitis
Mann J, Lucca L, Austin M, Merkin R, Robert M, Al Bawardy B, Raddassi K, Aizenbud L, Joshi N, Hafler D, Abraham C, Herold K, Kluger H. ScRNA-seq defines dynamic T-cell subsets in longitudinal colon and peripheral blood samples in immune checkpoint inhibitor-induced colitis. Journal For ImmunoTherapy Of Cancer 2023, 11: e007358. PMID: 37586769, PMCID: PMC10432652, DOI: 10.1136/jitc-2023-007358.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsImmune checkpoint inhibitorsT cell subsetsCheckpoint inhibitorsImmune environmentImmune checkpoint inhibitor-induced colitisCheckpoint inhibitor-induced colitisPeripheral immune environmentsStages of colitisTreatment of colitisMerkel cell carcinomaT cell populationsPeripheral blood samplesCourse of progressionT cell receptorMultiple tumor typesAlternative cancer therapyCommon toxicitiesICI colitisTreatment discontinuationAdverse eventsBiologic therapyImmune suppressionCell carcinomaColitisBlood samples
2021
The E3 ubiquitin ligase RNF186 and RNF186 risk variants regulate innate receptor-induced outcomes
Ranjan K, Hedl M, Abraham C. The E3 ubiquitin ligase RNF186 and RNF186 risk variants regulate innate receptor-induced outcomes. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2013500118. PMID: 34353900, PMCID: PMC8364215, DOI: 10.1073/pnas.2013500118.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsCytokinesHumansImmunity, InnateInflammatory Bowel DiseasesIntestinesMacrophagesMyeloid CellsNF-kappa BNod2 Signaling Adaptor ProteinPolymorphism, Single NucleotideReceptor-Interacting Protein Serine-Threonine Kinase 2Receptors, Pattern RecognitionToll-Like Receptor 2Toll-Like Receptor 4UbiquitinationUbiquitin-Protein LigasesConceptsPattern recognition receptorsE3 ubiquitin ligase activityStimulation of PRRsAntimicrobial reactive oxygen speciesMultiple pattern recognition receptorsLoss of functionLigase activityReactive nitrogen speciesComplex assemblyIntestinal myeloid cellsReactive oxygen speciesAutophagy pathwayDownstream signalingRNF186Bacterial clearanceRisk variantsRecognition receptorsHuman macrophagesOxygen speciesInnate immunityInflammatory bowel diseaseNitrogen speciesMicrobial clearanceSpeciesMyeloid cells
2020
Myeloid Cell Expression of LACC1 Is Required for Bacterial Clearance and Control of Intestinal Inflammation
Kang JW, Yan J, Ranjan K, Zhang X, Turner JR, Abraham C. Myeloid Cell Expression of LACC1 Is Required for Bacterial Clearance and Control of Intestinal Inflammation. Gastroenterology 2020, 159: 1051-1067. PMID: 32693188, PMCID: PMC8139320, DOI: 10.1053/j.gastro.2020.07.024.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCells, CulturedCoculture TechniquesColitis, UlcerativeCytokinesDextran SulfateDisease Models, AnimalDNA-Binding ProteinsFemaleHost Microbial InteractionsHumansImmunity, MucosalIntestinal MucosaIntracellular Signaling Peptides and ProteinsMaleMiceMice, KnockoutMyeloid CellsPrimary Cell CultureSalmonella InfectionsSalmonella typhimuriumConceptsIntestinal lymphoid organsBurden of bacteriaDextran sodium sulfateWild-type miceLymphoid organsTh17 cytokinesIntestinal inflammationDendritic cellsMyeloid cellsT cellsTh2 cytokinesMesenteric lymph node dendritic cellsLymph node dendritic cellsMyeloid cell-derived cytokinesAdaptive T cell responsesT cell transfer colitisMyeloid-specific disruptionInflammatory bowel diseaseReactive oxygen speciesImmune-mediated diseasesT cell responsesT helper 1Cell-derived cytokinesT cell cytokinesBone marrow-derived macrophagesT Cell-Intrinsic IRF5 Regulates T Cell Signaling, Migration, and Differentiation and Promotes Intestinal Inflammation
Yan J, Pandey SP, Barnes BJ, Turner JR, Abraham C. T Cell-Intrinsic IRF5 Regulates T Cell Signaling, Migration, and Differentiation and Promotes Intestinal Inflammation. Cell Reports 2020, 31: 107820. PMID: 32610123, PMCID: PMC7409536, DOI: 10.1016/j.celrep.2020.107820.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCell DifferentiationCell MovementColitisCytokinesGenetic Predisposition to DiseaseHumansInflammationInterferon Regulatory FactorsIntestinesLymph NodesMice, Inbred BALB CReceptors, Antigen, T-CellReceptors, ChemokineSignal TransductionT-LymphocytesUp-RegulationConceptsInflammatory outcomesTh17-associated transcription factorsMultiple immune-mediated diseasesPromotes Intestinal InflammationTh17-associated cytokinesAnti-inflammatory cytokinesImmune-mediated diseasesTh2-associated cytokinesChemokine-induced migrationExperimental colitisIntestinal inflammationUlcerative colitisHuman CD4IRF5 polymorphismsT cell signalingCytokinesCD4IRF5Th1Myeloid lineageGenetic carriersColitisCell migrationKey roleOutcomes
2019
LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes
Huang C, Hedl M, Ranjan K, Abraham C. LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes. Cell Reports 2019, 29: 4525-4539.e4. PMID: 31875558, PMCID: PMC7372507, DOI: 10.1016/j.celrep.2019.11.105.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsActivating Transcription Factor 6eIF-2 KinaseEndoplasmic ReticulumEndoplasmic Reticulum StressEndoribonucleasesEnterococcus faecalisEscherichia coliGene Expression RegulationHeLa CellsHost-Pathogen InteractionsHumansImmunity, InnateIntracellular Signaling Peptides and ProteinsMacrophagesNod2 Signaling Adaptor ProteinPhagocytosisPrimary Cell CultureProtein Serine-Threonine KinasesRiskSignal TransductionConceptsEndoplasmic reticulumER stressER stress sensorsHuman macrophagesInnate immune outcomesDisease risk variantsMultiple immune-mediated diseasesLaccase domainPattern recognition receptor NOD2HeLa cellsAntimicrobial pathwaysRisk variantsGenetic variantsLACC1Critical roleVariantsMacrophagesATF6IRE1αArg284SignalingReticulumStressTransfectionPERKIL23 induces IL23R recycling and amplifies innate receptor-induced signalling and cytokines in human macrophages, and the IBD-protective IL23R R381Q variant modulates these outcomes
Sun R, Hedl M, Abraham C. IL23 induces IL23R recycling and amplifies innate receptor-induced signalling and cytokines in human macrophages, and the IBD-protective IL23R R381Q variant modulates these outcomes. Gut 2019, 69: 264-273. PMID: 31097538, PMCID: PMC6858485, DOI: 10.1136/gutjnl-2018-316830.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMonocyte-derived macrophagesHuman monocyte-derived macrophagesJanus kinase/signal transducerKinase/signal transducerDynamin-mediated endocytosisReceptor-induced signalingCell surface regulationR381Q variantIBD pathogenesisIntestinal myeloid cellsLate endosomesPattern recognition receptorsSignal transducerPathway membersDefines mechanismsReal-time PCRCell typesHeLa cellsSignalingKey playersRNA expressionHuman macrophagesPathwayWestern blotMyeloid cells
2017
Human LACC1 increases innate receptor-induced responses and a LACC1 disease-risk variant modulates these outcomes
Lahiri A, Hedl M, Yan J, Abraham C. Human LACC1 increases innate receptor-induced responses and a LACC1 disease-risk variant modulates these outcomes. Nature Communications 2017, 8: 15614. PMID: 28593945, PMCID: PMC5472760, DOI: 10.1038/ncomms15614.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsBacteriaCells, CulturedCrohn DiseaseCytokinesElectron Transport Complex IIExtracellular Signal-Regulated MAP KinasesHumansImmunity, InnateIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMacrophagesNF-kappa BNod2 Signaling Adaptor Proteinp38 Mitogen-Activated Protein KinasesProteinsReactive Oxygen SpeciesReceptors, Pattern RecognitionRNA InterferenceRNA, Small InterferingSuccinate DehydrogenaseConceptsBacterial clearanceCytokine secretionDisease risk variantsReceptor-induced responsesMyeloid-derived cellsNOD2 stimulationRecognition receptorsHuman macrophagesSuccinate dehydrogenaseMtROS productionMitochondrial ROS productionROS productionOutcomesSDH activityMacrophagesSecretionFunctional consequencesClearanceLACC1PRRImportant contributorCellsDisease-associated lociReceptorsAn inflammatory bowel disease–risk variant in INAVA decreases pattern recognition receptor–induced outcomes
Yan J, Hedl M, Abraham C. An inflammatory bowel disease–risk variant in INAVA decreases pattern recognition receptor–induced outcomes. Journal Of Clinical Investigation 2017, 127: 2192-2205. PMID: 28436939, PMCID: PMC5451247, DOI: 10.1172/jci86282.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsActive Transport, Cell NucleusCarrier ProteinsCase-Control StudiesCytokinesEnterococcus faecalisGene ExpressionGenetic Association StudiesGenetic Predisposition to DiseaseHEK293 CellsHeterozygoteHumansInflammatory Bowel DiseasesMacrophagesMAP Kinase Signaling SystemMyeloid CellsPolymorphism, Single NucleotidePrimary Cell CultureReceptors, Pattern RecognitionRisk FactorsStaphylococcus aureusConceptsInflammatory bowel diseasePattern recognition receptor signalingDisease risk variantsIntestinal immune homeostasisActivation of MAPKIBD risk lociINAVAPrimary human cellsBacterial clearanceIntestinal myeloid cellsRisk lociAutophagy pathwayProper regulationIntronic regionsHuman cellsImmune homeostasisReceptor signalingDownstream signalsPRR stimulationReactive oxygenIntestinal microbesNF-κB activationGenesNF-κB pathwayMAPK
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Yale School of Medicine
Department of Medicine (Digestive Diseases), PO Box 208019
New Haven, CT 06520-8019
United States