Joshua Farber, DO
About
Appointments
Education & Training
- Addiction Psychiatry Fellowship
- Mount Sinai School of Medicine (2007)
- Psychiatry Residency
- New York Medical College (2005)
- Transitional Year Internship
- Flushing Hospital (2002)
- Physical Medicine and Rehabilitation Residency
- University of Medicine and Dentistry of New Jersey (2002)
- DO
- University of New England College of Osteopathic (2001)
- MA
- Boston University School of Medicine (1997)
- BS
- University of Connecticut, Physiology and Neurobiology (1996)
Research
Research at a Glance
Publications Timeline
A big-picture view of Joshua Farber's research output by year.
11Publications
1Citations
Publications
2023
Studies in humans and mice reveal a critical role for CCR2 in trafficking of pDCs during infection with SARS-CoV-2
Zhang H, Lu X, Garner D, Parween F, Singh S, Majumdar S, Weaver J, Stein S, Lesho P, Damcott C, Lutfi F, Petrick K, Rock P, Chertow D, Kelsall B, Murphy P, Dahiya S, Hardy N, Farber J. Studies in humans and mice reveal a critical role for CCR2 in trafficking of pDCs during infection with SARS-CoV-2. The Journal Of Immunology 2023, 210: 143.04-143.04. DOI: 10.4049/jimmunol.210.supp.143.04.Peer-Reviewed Original ResearchConceptsMAIT cellsSARS-CoV-2Chemokine receptorsCCR2-deficient miceHospitalized COVID-19 patientsCOVID-19 pathogenesisBlood pDCCOVID-19 patientsReporter miceAffecting disease severityCCR2 ligandsCCR2III interferonsBlood leukocytesType 1ChemokinesDisease severityIncreased mortalityBlood cellsReceptorsAbsolute numberLeukocyte extravasationLungTransendothelial migrationBloodExtravasation of pathogenic human type 17 Th cells requires both endothelial cell-bound and non-cell bound chemokines
Parween F, Singh S, Zhang H, Kathuria N, Farber J. Extravasation of pathogenic human type 17 Th cells requires both endothelial cell-bound and non-cell bound chemokines. The Journal Of Immunology 2023, 210: 79.07-79.07. DOI: 10.4049/jimmunol.210.supp.79.07.Peer-Reviewed Original ResearchConceptsEndothelial cellsTransendothelial migrationPro-inflammatory T cellsCCR2+ cellsMultiple chemokine receptorsHuman Th17 cellsImmune-mediated diseasesTransduced endothelial cellsBinding to endothelial cellsActivated endothelial cellsSites of inflammationActivity of receptorsTh17 signatureEndothelial cell surfaceTh17 cellsT cellsTh cellsChemokine receptorsGM-CSFCCR6Chemokine systemActivation of individual receptorsInhibition of transendothelial migrationApical sideTherapeutic benefit
2019
Keratinocyte-derived CCL20 orchestrates epidermal localization of IL-17-producing γδ T cells and ILCs to mediate psoriasis-like skin inflammation
Singh T, Lu X, Singh S, Zhang H, Doucet M, Kominsky S, Farber J. Keratinocyte-derived CCL20 orchestrates epidermal localization of IL-17-producing γδ T cells and ILCs to mediate psoriasis-like skin inflammation. The Journal Of Immunology 2019, 202: 183.21-183.21. DOI: 10.4049/jimmunol.202.supp.183.21.Peer-Reviewed Original ResearchConceptsIL-17-producingT cellsKnock-in miceIL-17Psoriasis-like skin inflammationGd T cellsExpression of CCL20Expression of IL17Hair folliclesCCR6 ligandIMQ treatmentPsoriatic dermatitisCCR6IL-22Skin inflammationReduce inflammationCCL20Day 4Treated skinInflammationMiceB-defensinsSuperficial epidermisKeratinocytesIMQ
2017
C/EBPd enables the efficient extravasation of human CCR2+ MAIT cells
Zhang H, Lee C, Too L, Singh S, Tsang H, Kabat J, Singh T, Farber J. C/EBPd enables the efficient extravasation of human CCR2+ MAIT cells. The Journal Of Immunology 2017, 198: 143.10-143.10. DOI: 10.4049/jimmunol.198.supp.143.10.Peer-Reviewed Original ResearchConceptsMAIT cellsHuman umbilical vein endothelial cellsT cellsHuman mucosal-associated invariant T (MAIT) cellsMucosal-associated invariant T (MAIT) cellsBZIP transcription factorsResponse to pathogen challengeHuman MAIT cellsCD8+ T cellsExpression of FUT7Activated human umbilical vein endothelial cellsChemokine receptor CCR6Non-redundant roleSelectin ligandsSites of inflammationPathogen challengeTranscription factorsUmbilical vein endothelial cellsMR1-restrictedCD8+Receptor CCR6Efficient extravasationInflamed skinVein endothelial cellsChemokine receptorsSingle-cell analysis of CCR6+ human Th cells reveals varying degrees of the type-17 phenotype, ranging from cells co-expressing to those fully suppressing opposing pathways
Singh S, Edara N, Zhang H, Chen J, Farber J. Single-cell analysis of CCR6+ human Th cells reveals varying degrees of the type-17 phenotype, ranging from cells co-expressing to those fully suppressing opposing pathways. The Journal Of Immunology 2017, 198: 150.14-150.14. DOI: 10.4049/jimmunol.198.supp.150.14.Peer-Reviewed Original ResearchConceptsType 17Co-expressionLineage-specific genesCo-expressed genesCells expressing various levelsTh cellsExpression of genesPattern of expressionSingle-cell analysisExpression of CCR6Opposing pathwaysMulti-lineage cellsGenesHuman Th cellsCells co-expressingLineagesDifferentiation in vivoCell sortingCCR6 expressionExpression levelsMemory populationIL-22IL-17A/FRT-PCRCCR6NOD2 deficiency exacerbates imiquimod-induced, psoriasis-like dermatitis
Singh T, Cipolla E, Singh S, Farber J. NOD2 deficiency exacerbates imiquimod-induced, psoriasis-like dermatitis. The Journal Of Immunology 2017, 198: 75.17-75.17. DOI: 10.4049/jimmunol.198.supp.75.17.Peer-Reviewed Original ResearchConceptsNucleotide-binding oligomerization domainNod2-/- micePsoriasis-like dermatitisToll-like receptorsIL-22Levels of mRNAPattern recognition proteinsIL-17AUp-regulation of NOD2Inhibition of Toll-like receptorImiquimod-treated skinRecognition proteinsDecreased levels of mRNAOligomerization domainAutoimmune skin diseaseIncreased levels of mRNAWild-type controlsExpression of mRNAInactivating mutationsAntibacterial defenseImiquimod-inducedNod2 deficiencyNOD2 functionT cellsIL-1ra
2014
Blood monocytes expressing CCR6 and monocyte-derived dendritic cells in dermis and epidermis are critical for IL-23-induced psoriasis-like inflammation in mice (CAM5P.238)
Singh T, Zhang H, Farber J. Blood monocytes expressing CCR6 and monocyte-derived dendritic cells in dermis and epidermis are critical for IL-23-induced psoriasis-like inflammation in mice (CAM5P.238). The Journal Of Immunology 2014, 192: 180.9-180.9. DOI: 10.4049/jimmunol.192.supp.180.9.Peer-Reviewed Original ResearchConceptsCCR6-/- miceIL-23 injectionDendritic cellsPsoriasis-like inflammationIL-23Blood monocytesAccumulation of dendritic cellsMonocyte-derived dendritic cellsHuman studiesLangerin-DTR micePsoriasis-like pathologyExpression of CCR6Monocyte-derived cellsLangerin+ cellsInflamed skinMyeloid cellsNon-monocyticIL-22Injected i.Psoriatic skinCCR6InflammationMiceMouse skinMonocytes
2011
Genetic deletion of chemokine receptor Ccr6 decreases atherogenesis in ApoE-deficient mice (117.2)
Wan W, Lim J, Lionakis M, Rivollier A, McDermott D, Kelsall B, Farber J, Murphy P. Genetic deletion of chemokine receptor Ccr6 decreases atherogenesis in ApoE-deficient mice (117.2). The Journal Of Immunology 2011, 186: 117.2-117.2. DOI: 10.4049/jimmunol.186.supp.117.2.Peer-Reviewed Original ResearchConceptsApoE-deficient miceCCR6-/- miceChemokine receptor CCR6Mice in vivoAtherosclerotic lesion areaApolipoprotein E-deficientApoE-/- miceReceptor CCR6Inflammatory monocytesLigand CCL20Monocyte functionCCR6Macrophage contentMonocyte levelsGenetic deletionPrimary monocytesLesional macrophagesWeeks of ageMouse monocytesMonocytesE deficiencyCCL20MiceMonocyte migrationCirculating blood
2010
Exaggerated IL-23-induced psoriasis-like inflammation in mice lacking CCR4 (135.32)
Hedrick M, Zhang H, Farber J. Exaggerated IL-23-induced psoriasis-like inflammation in mice lacking CCR4 (135.32). The Journal Of Immunology 2010, 184: 135.32-135.32. DOI: 10.4049/jimmunol.184.supp.135.32.Peer-Reviewed Original ResearchConceptsCCR4-deficient micePsoriasis-like inflammationT cellsIL-23Deficient miceIL-22Intradermal injection of IL-23Foxp3+ cellsExaggerated inflammatory responseWild-type miceIL-10 family cytokinesPro-inflammatory cytokinesIntramural Research ProgramIL-10 familyTh17 cellsTh2 cellsDendritic cellsIL-17AIL-17FMicroabscess formationChemokine receptorsInjected skinInfiltrating neutrophilsEffector functionsIntradermal injection
2009
Th17 Cells Are Not Required for Host Defense Against Murine Disseminated Candidiasis, But Are Required for Vaccine-Mediated Protection (132.10)
Lin L, Ibrahim A, Avanesian V, Xu X, Farber J, Fu Y, Baquir B, Spellberg B. Th17 Cells Are Not Required for Host Defense Against Murine Disseminated Candidiasis, But Are Required for Vaccine-Mediated Protection (132.10). The Journal Of Immunology 2009, 182: 132.10-132.10. DOI: 10.4049/jimmunol.182.supp.132.10.Peer-Reviewed Original ResearchCitationsConceptsCCR6-deficient miceDisseminated candidiasisVaccine-mediated protectionTh17 cellsIL-17Control miceRAls3p-NVaccine efficacyDeficient miceSusceptible to disseminated candidiasisCD4+IL-17+Wild type control miceMurine disseminated candidiasisRecombinant N-terminusLevels of IFNCompare Th1Th1/17 cellsT lymphocytesUnvaccinated miceC. albicansCandidiasisVaccinated miceTail veinTh17Candidal adhesin
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