Voluntary Faculty
Voluntary faculty are typically clinicians or others who are employed outside of the School but make significant contributions to department programs at the medical center or at affiliate institutions.
Voluntary rank detailsJoshua Farber, DO
Clinical InstructorAbout
Research
Publications
2025
Monitoring T-Cell Activation in the Tumor Microenvironment by PET Imaging of the Chemokine CXCL9.
Jacobson O, Zhang H, Olkowski C, Ghaemi B, Basuli F, Shi J, Bell M, Parween F, Ganesan S, Esparza T, Escorcia F, Choyke P, Farber J. Monitoring T-Cell Activation in the Tumor Microenvironment by PET Imaging of the Chemokine CXCL9. Journal Of Nuclear Medicine 2025, 66: 1372-1377. PMID: 40813232, PMCID: PMC12410298, DOI: 10.2967/jnumed.125.269795.Peer-Reviewed Original ResearchConceptsC-X-C motif chemokine ligand 9T cell activationT cell-engaging therapiesHumanized mouse modelT cellsTumor microenvironmentIFN-gXenograft modelGroup 1 innate lymphoid cellsEfficacy of cancer immunotherapyEngaging therapiesMethods:Biomarkers of immune activationTumor-to-background ratioResults:PET imagingResponse to immunotherapyTumor-to-backgroundImmune-mediated diseasesMonitoring of immune responsesSubcutaneous xenograft modelChemokine ligand 9Monitoring T-cell activationNoninvasive visualizationNoninvasive monitoringMigration arrest and transendothelial trafficking of human pathogenic-like Th17 cells are mediated by differentially positioned chemokines
Parween F, Singh S, Kathuria N, Zhang H, Ashida S, Otaizo-Carrasquero F, Shamsaddini A, Gardina P, Ganesan S, Kabat J, Lorenzi H, Riley D, Myers T, Pittaluga S, Bielekova B, Farber J. Migration arrest and transendothelial trafficking of human pathogenic-like Th17 cells are mediated by differentially positioned chemokines. Nature Communications 2025, 16: 1978. PMID: 40000641, PMCID: PMC11861662, DOI: 10.1038/s41467-025-57002-6.Peer-Reviewed Original ResearchConceptsEndothelial cellsTransendothelial migrationCCR2 ligandsFunction of CCR6Migration arrestChemokine receptor CCR6T cell receptor activationCerebrospinal fluid of patientsActivation-associated genesFluid of patientsActivated endothelial cellsEC surfaceTh17 signatureReceptor CCR6Th17 cellsT cellsChemokine receptorsCell extravasationInflammatory cytokinesReceptor activationCerebrospinal fluidCCR6ChemokinesMultiple sclerosisEnhanced expression
2024
Comparative Kidney Uptake of Nanobody-Based PET Tracers Labeled with Various Fluorine-18-Labeled Prosthetic Groups
Olkowski C, Basuli F, Fernandes B, Ghaemi B, Shi J, Zhang H, Farber J, Escorcia F, Choyke P, Jacobson O. Comparative Kidney Uptake of Nanobody-Based PET Tracers Labeled with Various Fluorine-18-Labeled Prosthetic Groups. Molecular Pharmaceutics 2024, 22: 533-543. PMID: 39680709, DOI: 10.1021/acs.molpharmaceut.4c01101.Peer-Reviewed Original ResearchCxcl10 is protective during mouse-adapted SARS-CoV-2 infection
Majumdar S, Weaver J, Pontejo S, Minai M, Lu X, Gao J, Holmes G, Johnson R, Zhang H, Kelsall B, Farber J, Alves D, Murphy P. Cxcl10 is protective during mouse-adapted SARS-CoV-2 infection. Journal Of Leukocyte Biology 2024, 117: qiae252. PMID: 39607906, PMCID: PMC11953068, DOI: 10.1093/jleuko/qiae252.Peer-Reviewed Original ResearchSARS-CoV-2 infectionSARS-CoV-2Mouse-adapted strain of SARS-CoV-2Absence of CXCL10Associated with poor outcomesCXCL10-/- miceLungs of male miceInflammatory gene inductionAcute SARS-CoV-2 infectionMouse-adapted strainSevere COVID-19Wild type controlsCXCL10-deficientChemokine CXCL10Lymphocytic infiltrationSevere acute respiratory syndrome coronavirus 2Poor outcomeAcute respiratory syndrome coronavirus 2Circulating LevelsMale miceRespiratory syndrome coronavirus 2Infected miceSARS-CoV-2 pathogenesisVirus loadCXCL10
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 ResearchMAIT 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 ResearchEndothelial 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 ResearchIL-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 ResearchMAIT 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 ResearchType 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 ResearchNucleotide-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