Vikki M Abrahams, PhD
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Director, Division of Reproductive Sciences, Department of Obstetrics, Gynecology & Reproductive Sciences; Co-Vice Chair of Faculty Development, Department of Obstetrics, Gynecology & Reproductive Sciences
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Director, Division of Reproductive Sciences, Department of Obstetrics, Gynecology & Reproductive Sciences; Co-Vice Chair of Faculty Development, Department of Obstetrics, Gynecology & Reproductive Sciences
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Appointments
Titles
Director, Division of Reproductive Sciences, Department of Obstetrics, Gynecology & Reproductive Sciences; Co-Vice Chair of Faculty Development, Department of Obstetrics, Gynecology & Reproductive Sciences
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Professor, Obstetrics, Gynecology & Reproductive Sciences
Director, Division of Reproductive Sciences, Department of Obstetrics, Gynecology & Reproductive Sciences; Co-Vice Chair of Faculty Development, Department of Obstetrics, Gynecology & Reproductive SciencesBiography
Dr Vikki Abrahams is a Professor, Director of the Division of Reproductive Sciences and Co-Vice Chair of Faculty Development in the Department of Obstetrics, Gynecology and Reproductive Sciences.
Dr Abrahams received her B.Sc. (hons) in Immunology in 1996, and was awarded a Ph.D. in Immunology in 2000, both from University College London. She continued her studies as a postdoctoral associate at Dartmouth Medical School and then at Yale University in the field of Reproductive Immunology. In 2004 she joined the faculty in the Department of Obstetrics, Gynecology and Reproductive Sciences at Yale School of Medicine.
Dr Abrahams' research focuses on understanding the role of innate immune Toll-like receptor and Nod-like receptor family members in placental and maternal-fetal immune responses, and their role in regulating pregnancy outcome, including those complicated by infections and by autoimmune diseases. Studies from the Abrahams laboratory has characterized the mechanisms by which Toll-like receptors, Nod-like receptors, and the inflammasome function in the placental trophoblast and fetal membranes in response to both infectious and non-infectious stimuli.
Dr Abrahams is a member of the American Association of Immunologists, International Society for Immunology of Reproduction, Society for Reproductive Investigation, and the American Society of Reproductive Immunology. Dr Abrahams is the Associate Editor for Reviews of the American Journal of Reproductive Immunology and also serves on the editorial boards for a number of other journals within the Reproductive Sciences field.
Appointments
Obstetrics, Gynecology & Reproductive Sciences
ProfessorPrimary
Other Departments & Organizations
- Abrahams Lab
- Discovery to Cure Internship
- Human and Translational Immunology Program
- Obstetrics, Gynecology & Reproductive Sciences
- Perinatal Research
- Reproductive Sciences
- Yale WRHR Advisory Committee
Education & Training
- PhD
- University College (2000)
Research
Overview
Medical Subject Headings (MeSH)
Antibodies, Antiphospholipid; Antiphospholipid Syndrome; Autoimmune Diseases; Exosomes; Fetal Membranes, Premature Rupture; Immunity, Innate; Inflammasomes; MicroRNAs; Nod Signaling Adaptor Proteins; Placenta; Pregnancy Complications; Pregnancy Complications, Infectious; Pregnancy in Diabetics; Toll-Like Receptors
ORCID
0000-0003-4995-1061
Research at a Glance
Yale Co-Authors
Frequent collaborators of Vikki M Abrahams's published research.
Publications Timeline
A big-picture view of Vikki M Abrahams's research output by year.
Research Interests
Research topics Vikki M Abrahams is interested in exploring.
Mancy Tong, PhD
Seth Guller, PhD
Crina Boeras
Alyssa Ann Grimshaw, MBA, MLIS, MPH
Michael Paidas, MD
Shannon Whirledge, PhD, MSc
29Publications
785Citations
Antibodies, Antiphospholipid
Inflammasomes
Antiphospholipid Syndrome
MicroRNAs
Placenta
Toll-Like Receptors
Publications
2024
Antiphospholipid-exposed trophoblast-derived extracellular vesicles express elevated levels of TLR7/8-activating microRNAs and induce endometrial endothelial activation, in part, through TLR7
Coenen C, Hidalgo T, Lynn T, Jones D, Salmon J, Chamley L, Abrahams V. Antiphospholipid-exposed trophoblast-derived extracellular vesicles express elevated levels of TLR7/8-activating microRNAs and induce endometrial endothelial activation, in part, through TLR7. Journal Of Reproductive Immunology 2024, 164: 104255. PMID: 38797133, DOI: 10.1016/j.jri.2024.104255.Peer-Reviewed Original ResearchConceptsHuman endometrial endothelial cellsObstetric antiphospholipid syndromeToll-like receptor 4MiR-146a-3pMaternal-fetal interfaceAntiphospholipid syndromeIL-8 responseEndometrial endothelial cellsTrophoblast cellsExtracellular vesiclesElevated levels of IL-8IL-8Endothelial cellsLevels of IL-8Activation of Toll-like receptor 4Downstream of toll-like receptor 4Exposure to aPLElevated levelsExtravillous trophoblast cellsHuman trophoblast cellsInsufficient placentationTrophoblast-derived extracellular vesiclesAntiphospholipid antibodiesMaternal vasculaturePlacental trophoblastsTLR8‐activating miR‐146a‐3p is an intermediate signal contributing to fetal membrane inflammation in response to bacterial LPS
Georges H, Cassin C, Tong M, Abrahams V. TLR8‐activating miR‐146a‐3p is an intermediate signal contributing to fetal membrane inflammation in response to bacterial LPS. Immunology 2024, 172: 577-587. PMID: 38631842, PMCID: PMC11223956, DOI: 10.1111/imm.13794.Peer-Reviewed Original ResearchAltmetricConceptsMiR-146a-3pPreterm birthFetal membranesToll-like receptorsExpression of miR-146a-3pLipopolysaccharide exposureMouse model of pregnancyIL-8Response to bacterial LPSAssociated with chorioamnionitisFetal membrane inflammationHuman FM explantsMouse fetal membranesInduced preterm birthBacterial lipopolysaccharideMaternal-fetal interfaceDanger signalsWild-type miceIn vivo mouse modelModel of pregnancyInterleukin (IL)-8Pro-inflammatory roleResponse to bacterial lipopolysaccharideAssociated with elevated levelsResponse to LPS
2023
Decidualization dampens toll-like receptor mediated inflammatory responses in human endometrial stromal cells by upregulating IκBα
Tong M, Scott J, Whirledge S, Abrahams V. Decidualization dampens toll-like receptor mediated inflammatory responses in human endometrial stromal cells by upregulating IκBα. Journal Of Reproductive Immunology 2023, 159: 103988. PMID: 37451159, PMCID: PMC10530124, DOI: 10.1016/j.jri.2023.103988.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsEndometrial stromal cellsInflammatory responseStromal cellsHuman endometrial stromal cellsToll-like receptor signalingSex hormone levelsMenstrual cycle stageToll-like receptorsImmune response changesViral double-stranded RNAHuman EnSCsEndometrial responseProinflammatory cytokinesSuccessful pregnancyMenstrual cycleHuman endometriumHormone levelsMajor cell typesImmune responseNFκB p65Viral infectionDecidualizationBacterial lipopolysaccharideReceptor signalingBacterial componentsEndometrial responses to bacterial and viral infection: a scoping review.
Lindsay C, Potter J, Grimshaw A, Abrahams V, Tong M. Endometrial responses to bacterial and viral infection: a scoping review. Human Reproduction Update 2023, 29: 675-693. PMID: 37290428, PMCID: PMC10477945, DOI: 10.1093/humupd/dmad013.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsEndometrial responseViral infectionUterus/endometriumFull-text studiesInnate immune sensingInnate immune responseFree-text termsEmbase/MedlineIntrauterine infectionObstetric complicationsEndometrial productionCochrane LibraryFuture studiesImplantation failureNeisseria gonorrheaImmune cellsMost infectionsImmune responseUterine functionChlamydia trachomatisAnimal modelsImmune sensingEndometriumZika virusMajority of studiesCell-free fetal DNA impairs trophoblast migration in a TLR9-dependent manner and can be reversed by hydroxychloroquine
León-Martínez D, Lynn T, Abrahams V. Cell-free fetal DNA impairs trophoblast migration in a TLR9-dependent manner and can be reversed by hydroxychloroquine. Journal Of Reproductive Immunology 2023, 157: 103945. PMID: 37062109, DOI: 10.1016/j.jri.2023.103945.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsToll-like receptor 9Aspirin-triggered lipoxinsODN 2216Pathogenesis of preeclampsiaTLR9-dependent mannerNovel therapeutic approachesTrophoblast cell modelReceptor 9CpG oligodeoxynucleotideTLR9 inhibitorPlacental functionTherapeutic approachesCell-free fetal DNACpG motifsTherapeutic agentsHCQPreeclampsiaHydroxychloroquineFetal DNACell viabilityCffDNAMolecular underpinningsCell modelInhibitionASA
2022
Distinct non‐coding RNA cargo of extracellular vesicles from M1 and M2 human primary macrophages
Pantazi P, Clements T, Venø M, Abrahams V, Holder B. Distinct non‐coding RNA cargo of extracellular vesicles from M1 and M2 human primary macrophages. Journal Of Extracellular Vesicles 2022, 11: 12293. PMID: 36544271, PMCID: PMC9772496, DOI: 10.1002/jev2.12293.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsNon-coding RNAsSmall non-coding RNAsY RNA fragmentsTRNA fragmentsRNA cargoExtracellular vesiclesFull-length tRNASmall RNA sequencingPrimary macrophagesSmall RNA cargoHigh relative abundanceHuman primary macrophagesRNA sequencingEnrichment analysisGene targetsGene expressionFirst comprehensive analysisSignaling pathwaysFunctional cargoRelative abundanceLow abundancePutative roleRNASnoRNAsInflammatory signaling pathwaysThe serotonin reuptake inhibitor fluoxetine induces human fetal membrane sterile inflammation through p38 MAPK activation
Fabrizio V, Lindsay C, Wilcox M, Hong S, Lynn T, Norwitz E, Yonkers K, Abrahams V. The serotonin reuptake inhibitor fluoxetine induces human fetal membrane sterile inflammation through p38 MAPK activation. Journal Of Reproductive Immunology 2022, 155: 103786. PMID: 36528909, PMCID: PMC9851981, DOI: 10.1016/j.jri.2022.103786.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAntidepressive AgentsExtraembryonic MembranesFemaleFetal Membranes, Premature RuptureFluoxetineHumansHydroxymethylglutaryl-CoA Reductase InhibitorsInfant, NewbornInflammationInterleukin-6P38 Mitogen-Activated Protein KinasesPregnancyPremature BirthSelective Serotonin Reuptake InhibitorsConceptsSerotonin reuptake inhibitorsP38 MAPK activitySerotonin reuptake inhibitor fluoxetineSubsequent preterm birthFirst-line therapyPreterm premature ruptureReuptake inhibitor fluoxetineInflammatory IL-6Normal term deliveryIL-6 productionIL-6 secretionFetal membrane inflammationUnexposed womenAntidepressant treatmentLine therapyPreterm birthAntidepressant useReuptake inhibitorsTerm deliveryMembrane inflammationPremature ruptureIL-6SRI useSterile inflammationP38 MAPK pathwayPlacental macrophage responses to viral and bacterial ligands and the influence of fetal sex
Pantazi P, Kaforou M, Tang Z, Abrahams V, McArdle A, Guller S, Holder B. Placental macrophage responses to viral and bacterial ligands and the influence of fetal sex. IScience 2022, 25: 105653. PMID: 36505933, PMCID: PMC9732417, DOI: 10.1016/j.isci.2022.105653.Peer-Reviewed Original ResearchCitationsAltmetricConceptsPathogen-associated molecular patternsViral pathogen-associated molecular patternsHofbauer cellsFetal sexMajor histocompatibility complex class IAdverse pregnancy outcomesHistocompatibility complex class IToll-like receptorsComplex class ISex-dependent responseInfectious triggerPregnancy outcomesPlacental macrophagesVertical pathogen transmissionViral infectionLipid metabolismMacrophage responseBacterial ligandsProtein expression changesClass IMolecular patternsPlacentaMacrophagesCytoskeleton organizationQuantitative proteomicsEditorial: Translational Virology in Pregnancy
Waldorf K, Abrahams V. Editorial: Translational Virology in Pregnancy. Frontiers In Virology 2022, 2: 908471. PMID: 36313916, PMCID: PMC9611285, DOI: 10.3389/fviro.2022.908471.Peer-Reviewed Original ResearchAltmetric
2019
Lipopolysaccharide-Stimulated Human Fetal Membranes Induce Neutrophil Activation and Release of Vital Neutrophil Extracellular Traps.
Tong M, Potter JA, Mor G, Abrahams VM. Lipopolysaccharide-Stimulated Human Fetal Membranes Induce Neutrophil Activation and Release of Vital Neutrophil Extracellular Traps. The Journal Of Immunology 2019, 203: 500-510. PMID: 31167775, PMCID: PMC6616008, DOI: 10.4049/jimmunol.1900262.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsNeutrophil extracellular trapsNeutrophil recruitmentFetal membranesReactive oxygen species productionPreterm birthExtracellular trapsOxygen species productionCytokine/chemokine secretionChemokine/cytokine productionMajor risk factorSpecies productionBacterial LPS stimulationNeutrophil infiltrationProinflammatory factorsFetal interfaceChemokine secretionNeonatal mortalityCytokine productionNeutrophil activationRisk factorsTissue injuryNeutrophil viabilityLPS stimulationEx vivoNET formation
Academic Achievements and Community Involvement
activity Member
Professional OrganizationsAmerican Society for Reproductive ImmunologyDetails05/01/2000 - Presentactivity Member
Professional OrganizationsAmerican Association of ImmunologistsDetails2009 - Presentactivity Member
CommitteesAssociate Editor for Reviews for the American Journal of Reproductive ImmunologyDetails07/01/2010 - Presentactivity Member
CommitteesEditorial Board for the Journal of Reproductive ImmunologyDetails07/01/2006 - Presentactivity Member
Professional OrganizationsThe International Society for Immunology of ReproductionDetails07/01/2011 - Present
Links & Media
News
- May 16, 2023
Women’s Health Research at Yale Funds Studies to Improve Early Detection of Ovarian Cancer, Treatment of Prenatal Infections, and Aortic Aneurysm Outcomes in Women
- April 13, 2023
Research Adds Insights Into Preeclampsia, a Deadly Pregnancy Complication
- December 14, 2022Source: YaleNews
Inflammation May Explain Antidepressants’ Link to Preterm Birth
- May 26, 2022Source: YaleNews
Shedding light on the link between a type of antibodies and miscarriage