2023
Extravasation 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 receptorsNOD2 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
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 ResearchCCR4-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
2007
CCR2 identifies first responders among human CD4+ memory T cells: long-lived, apoptosis-resistant, antigen-responsive cells with enhanced migration potential, a low threshold for activation, and immediate effector capabilities (85.5)
Farber J, Song K, Zhang H, Rabin R, Hill B, Sereti I, Prussin C, Siegel R, Douek D, Roederer M. CCR2 identifies first responders among human CD4+ memory T cells: long-lived, apoptosis-resistant, antigen-responsive cells with enhanced migration potential, a low threshold for activation, and immediate effector capabilities (85.5). The Journal Of Immunology 2007, 178: s119-s119. DOI: 10.4049/jimmunol.178.supp.85.5.Peer-Reviewed Original ResearchMemory T cellsT cellsEffector capabilitiesExpression of chemokine receptors CCR5Memory CD4+ T cellsCD4+ memory T cellsCD4+ T cellsLong-lived memory cellsHuman memory CD4+ T cellsCCR2+ cellsCD4+ subsetHuman CD4+ memory T cellsChemokine receptor CCR5Antigen-responsive cellsChemokine receptor typeResistance to apoptosisSecrete high levelsCells co-expressingSusceptibility to apoptosisReduced proliferative potentialEffector cytokinesExcision circlesEnhanced migration potentialReceptor CCR5Peripheral blood