2023
HIF-1 regulates pathogenic cytotoxic T cells in lupus skin disease
Little A, Chen P, Vesely M, Khan R, Fiedler J, Garritano J, Islam F, McNiff J, Craft J. HIF-1 regulates pathogenic cytotoxic T cells in lupus skin disease. JCI Insight 2023, 8: e166076. PMID: 37526979, PMCID: PMC10543720, DOI: 10.1172/jci.insight.166076.Peer-Reviewed Original ResearchConceptsCutaneous lupus erythematosusLupus skin diseaseT cellsSkin diseasesCytotoxic signatureInflammatory infiltrateHIF-1Tissue damageKidney-infiltrating T cellsSkin-infiltrating T cellsAutoimmune skin diseaseHIF-1 inhibitionSkin tissue damageLupus erythematosusSystemic diseaseTissue inflammationGranzyme BMouse modelInflammatory gene programDiseaseProtein levelsInfiltratesSkin environmentGene programPresent study
2013
PD-L1 and PD-L2 Protect The Heart In a T-Cell Receptor Transgenic Model Of Graft-Versus Host Disease
Juchem K, Anderson B, Zhang C, Sharpe A, McNiff J, Demetris A, Shlomchik M, Shlomchik W. PD-L1 and PD-L2 Protect The Heart In a T-Cell Receptor Transgenic Model Of Graft-Versus Host Disease. Blood 2013, 122: 4479. DOI: 10.1182/blood.v122.21.4479.4479.Peer-Reviewed Original ResearchDonor bone marrowPD-L1PD-L1/2T cellsBone marrowLate weight lossWeight lossHost diseasePD-1Graft Versus Host DiseaseInhibitory molecules PD-1Effector memory T cellsT cell receptor transgenic modelAllogeneic stem cell transplantationT-cell-mediated pathogenesisMore chronic phasesPD-L1/2 expressionRadioresistant stromal cellsDays post transplantHost T cellsCD4 T cellsMemory T cellsStem cell transplantationNaive T cellsEarly weight loss
2011
A repertoire independent and cell intrinsic defect in murine GVHD induction by effector memory T cells (169.6)
Juchem K, Anderson B, Zhang C, McNiff J, Demetris A, Caton A, Shlomchik W, Shlomchik M. A repertoire independent and cell intrinsic defect in murine GVHD induction by effector memory T cells (169.6). The Journal Of Immunology 2011, 186: 169.6-169.6. DOI: 10.4049/jimmunol.186.supp.169.6.Peer-Reviewed Original ResearchMemory T cellsEffector memory T cellsT cellsGVHD inductionAllogeneic stem cell transplantationMemory T cell poolCentral memory T cellsT cell receptor transgenicT cell receptor repertoireT cell poolStem cell transplantationCell receptor repertoireNaïve T cellsTg T cellsSyngeneic bone marrowCell-intrinsic defectTransient GVHDHost diseasePost transplantMajor complicationsPD-1PD-L1Transgenic recipientsCell transplantationNaive CD4
2009
A New TCR Transgenic Model of GVHD Reveals That, Independent of Repertoire, Effector Memory T Cells Are Severely Limited, and Central Memory T Cells Somewhat Limited, in Their Ability to Cause GVHD.
Wilkinson K, Anderson B, McNiff J, Demetris A, Shlomchik W, Shlomchik M. A New TCR Transgenic Model of GVHD Reveals That, Independent of Repertoire, Effector Memory T Cells Are Severely Limited, and Central Memory T Cells Somewhat Limited, in Their Ability to Cause GVHD. Blood 2009, 114: 233. DOI: 10.1182/blood.v114.22.233.233.Peer-Reviewed Original ResearchEM T cellsCD4 T cellsCM CD4 T cellsCM T cellsDays post transplantMemory T cellsTCR transgenic modelT cellsPost transplantTs1 cellsLymph nodesCell recipientsWeight lossTransgenic modelCentral memory CD4 T cellsEffector memory T cellsAllogeneic stem cell transplantationMemory CD4 T cellsT cell receptor repertoireCentral memory TContext of GVHDInduction of GVHDInitiation of GVHDModel of GVHDRAG-deficient backgroundDonor APCs Promote Gvhd in MHC-Mismatched Transplants by Indirectly Presenting Host Minor Histocompatibility Antigens.
Wang X, Martone C, Demetris A, McNiff J, Shlomchik W. Donor APCs Promote Gvhd in MHC-Mismatched Transplants by Indirectly Presenting Host Minor Histocompatibility Antigens. Blood 2009, 114: 689. DOI: 10.1182/blood.v114.22.689.689.Peer-Reviewed Original ResearchAntigen presenting cellsBALB/c miceHost minor histocompatibility antigensCD4 cellsMinor histocompatibility antigensT cellsC miceAcute GVHDAllogeneic MHCChronic GVHDDonor BMHistocompatibility antigensIndirect presentationFemale recipientsT cell receptor transgenic T cellsDay 7Bone marrow/stem cell transplantationFemale BALB/c miceHost antigen presenting cellsMale BALB/c miceRecipient antigen presenting cellsBALB/c modelAlloreactive CD4 cellsPrime T cellsStem cell transplantation
2008
Redundant Mechanisms for Dendritic Cell Activation in GVHD Induction: Signalings Via TLRs, TNF-α, IL-1 and CD40 Are Not Required
Li H, Matte-Martone C, Demetris A, McNiff J, Jain D, Shlomchik W. Redundant Mechanisms for Dendritic Cell Activation in GVHD Induction: Signalings Via TLRs, TNF-α, IL-1 and CD40 Are Not Required. Blood 2008, 112: 3509. DOI: 10.1182/blood.v112.11.3509.3509.Peer-Reviewed Original ResearchHost antigen-presenting cellsAntigen-presenting cellsToll-like receptorsDC maturation signalsDonor T cellsDendritic cellsT cellsT cell activationMaturation signalsCell activationGVHD inductionHistologic GVHDMyD88/DC maturationAPC maturationIL-1Alloreactive donor T cellsAlloreactive T cell activationAdaptive T cell responsesAllogeneic stem cell transplantationHost hematopoietic cellsTNFR1/R2WT B6 miceDendritic cell activationT cell primingRecipient Langerhans Cells Are Neither Required Nor Sufficient for GVHD Induction in MHC-Matched Allogeneic BMT, but a Langerin+ Cell Is a Pivotal Regulator of Langerhans Cell Turnover Post Transplantation
Li H, Kaplan D, Demetris A, McNiff J, Shlomchik M, Shlomchik W. Recipient Langerhans Cells Are Neither Required Nor Sufficient for GVHD Induction in MHC-Matched Allogeneic BMT, but a Langerin+ Cell Is a Pivotal Regulator of Langerhans Cell Turnover Post Transplantation. Blood 2008, 112: 3511. DOI: 10.1182/blood.v112.11.3511.3511.Peer-Reviewed Original ResearchRecipient antigen-presenting cellsHost Langerhans cellsAntigen-presenting cellsBone marrow transplantAllogeneic bone marrow transplantRecipient Langerhans cellsDonor T cellsGVHD inductionEpidermal Langerhans cellsLangerhans cellsBone marrowSkin GVHDMarrow transplantT cellsAllogeneic donor T cellsAlloreactive donor T cellsDonor-derived Langerhans cellsMajor antigen-presenting cellsHost antigen-presenting cellsProfessional antigen-presenting cellsWeight lossDonor Langerhans cellsExpression of langerinTime of transplantUV-induced inflammation
2005
CD8+ but Not CD4+ T Cells Require Cognate Interactions with Target Tissues To Mediate GVHD across Only Minor H Antigens but CD4+ and CD8+ T Cells Both Require Direct Leukemic Contact for GVL.
Shlomchik W, Matte C, Liu J, Jain D, McNiff J. CD8+ but Not CD4+ T Cells Require Cognate Interactions with Target Tissues To Mediate GVHD across Only Minor H Antigens but CD4+ and CD8+ T Cells Both Require Direct Leukemic Contact for GVL. Blood 2005, 106: 580. DOI: 10.1182/blood.v106.11.580.580.Peer-Reviewed Original ResearchCD8-mediated GVHDDirect cognate interactionT cellsSecond transplantCD4 cellsCD8 cellsHost antigensCognate interactionMHCII expressionBone marrowDonor CD4 cellsDonor-derived APCsTarget tissuesT-cell releaseAlloreactive T cellsBone marrow chimerasMinor H antigensCognate T cellsChimeric recipientsDonor BMGVHD lethalityHistologic GVHDHost APCsLess GVHDLeukemic expression
2001
Pathogenesis of autoimmunity in αβ T cell-deficient lupus-prone mice
Peng S, Cappadona J, Mcniff J, Madaio M, Owen M, Hayday A, Craft J. Pathogenesis of autoimmunity in αβ T cell-deficient lupus-prone mice. Clinical & Experimental Immunology 2001, 111: 107-116. PMID: 9472669, PMCID: PMC1904839, DOI: 10.1046/j.1365-2249.1998.00424.x.Peer-Reviewed Original ResearchConceptsT cell-dependent mechanismCell-dependent mechanismEnd-organ diseaseImmune complex depositionGammadelta T cellsRenal diseaseMurine lupusComplex depositionT cellsMRL miceSkin lesionsComplement fixationT-cell-deficient animalsEnd-organ damageLupus-prone miceNon-autoimmune micePathogenesis of autoimmunityYears of ageHumoral autoimmunityLupus lesionsAutoantibody productionSkin diseasesSkin injuryTCR alphaFas antigenSelective T-cell subset ablation demonstrates a role for T1 and T2 cells in ongoing acute graft-versus-host disease: a model system for the reversal of disease
Liu J, Anderson B, Robert M, McNiff J, Emerson S, Shlomchik W, Shlomchik M. Selective T-cell subset ablation demonstrates a role for T1 and T2 cells in ongoing acute graft-versus-host disease: a model system for the reversal of disease. Blood 2001, 98: 3367-3375. PMID: 11719376, DOI: 10.1182/blood.v98.12.3367.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DeathCytokinesDisease Models, AnimalFlow CytometryGanciclovirGraft vs Host DiseaseGraft vs Leukemia EffectHematopoiesisHematopoietic Stem CellsInterleukin-2Interleukin-4Lymphocyte SubsetsMaleMiceMice, TransgenicPromoter Regions, GeneticSimplexvirusSpleenThymidine KinaseThymus GlandT-LymphocytesWeight GainConceptsDonor T cellsT cellsT2 cellsGVHD reactionsHost diseaseInterleukin-2Herpes simplex virus thymidine kinase gene transductionAllogeneic stem cell transplantationCytokine-producing T cellsPrevention of GVHDStem cell transplantationReversal of diseaseT cell deletionLater time pointsAcute graftCytokine polarizationOngoing GVHDClinical GVHDAntibody infusionPeak diseaseClinical effectsCell transplantationIL-4 promoterGVHDDeficient miceDeficiency in β2-Microglobulin, But Not CD1, Accelerates Spontaneous Lupus Skin Disease While Inhibiting Nephritis in MRL-Faslpr Mice: An Example of Disease Regulation at the Organ Level
Chan O, Paliwal V, McNiff J, Park S, Bendelac A, Shlomchik M. Deficiency in β2-Microglobulin, But Not CD1, Accelerates Spontaneous Lupus Skin Disease While Inhibiting Nephritis in MRL-Faslpr Mice: An Example of Disease Regulation at the Organ Level. The Journal Of Immunology 2001, 167: 2985-2990. PMID: 11509649, DOI: 10.4049/jimmunol.167.5.2985.Peer-Reviewed Original ResearchConceptsSkin diseasesT cell-dependent mechanismMRL/lpr miceLupus skin diseaseLupus skin lesionsMRL-Faslpr miceNonclassical MHC moleculesTarget organ diseaseCell-dependent mechanismTarget organ levelRegulation of autoimmunitySecondary lymphoid tissuesAutoreactive lymphocytesMurine lupusLpr miceSystemic diseaseAutoimmune diseasesLymphoid tissueOrgan diseaseDeficient miceT cellsSkin lesionsEnd organsOrgan levelImmune system
1999
Prevention of Graft Versus Host Disease by Inactivation of Host Antigen-Presenting Cells
Shlomchik W, Couzens M, Tang C, McNiff J, Robert M, Liu J, Shlomchik M, Emerson S. Prevention of Graft Versus Host Disease by Inactivation of Host Antigen-Presenting Cells. Science 1999, 285: 412-415. PMID: 10411505, DOI: 10.1126/science.285.5426.412.Peer-Reviewed Original ResearchConceptsAntigen-presenting cellsAllogeneic bone marrow transplantationBone marrow transplantationHost diseaseMarrow transplantationT cellsMurine allogeneic bone marrow transplantation modelAllogeneic bone marrow transplantation modelHost-derived antigen-presenting cellsGraft Versus Host DiseaseHost antigen-presenting cellsDonor antigen-presenting cellsVersus Host DiseaseDonor T cellsAllogeneic T cellsBone marrow transplantation modelAlloimmune attackHost antigensTransplantation modelImportant toxicityNeoplastic diseaseDiseaseGraftTransplantationHost tissuesExtracorporeal photochemotherapy in human and murine graft-versus-host disease
Girardi M, McNiff J, Heald P. Extracorporeal photochemotherapy in human and murine graft-versus-host disease. Journal Of Dermatological Science 1999, 19: 106-113. PMID: 10098701, DOI: 10.1016/s0923-1811(98)00066-8.Peer-Reviewed Original Research
1998
Dermal Microvascular Injury in the Human Peripheral Blood Lymphocyte Reconstituted-Severe Combined Immunodeficient (HuPBL-SCID) Mouse/Skin Allograft Model Is T Cell Mediated and Inhibited by a Combination of Cyclosporine and Rapamycin
Murray A, Schechner J, Epperson D, Sultan P, McNiff J, Hughes C, Lorber M, Askenase P, Pober J. Dermal Microvascular Injury in the Human Peripheral Blood Lymphocyte Reconstituted-Severe Combined Immunodeficient (HuPBL-SCID) Mouse/Skin Allograft Model Is T Cell Mediated and Inhibited by a Combination of Cyclosporine and Rapamycin. American Journal Of Pathology 1998, 153: 627-638. PMID: 9708821, PMCID: PMC1852982, DOI: 10.1016/s0002-9440(10)65604-0.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsB-LymphocytesCD8-Positive T-LymphocytesCyclosporineDrug Therapy, CombinationEndothelium, VascularEnzyme-Linked Immunosorbent AssayFlow CytometryGenes, MHC Class IIGraft RejectionHumansImmunosuppressive AgentsKeratinocytesMiceMice, SCIDMicrocirculationPolyenesSirolimusSkinSkin TransplantationT-LymphocytesTransplantation, HomologousVascular Cell Adhesion Molecule-1ConceptsPeripheral blood mononuclear cellsHuman peripheral blood mononuclear cellsSkin allograft modelMicrovascular injuryT cellsCell infiltrateAllograft modelWhole peripheral blood mononuclear cellsT cell-dependent mechanismT cell-mediated rejectionHuman natural killer cellsSCID/beige miceEndothelial cell sloughingT Cell-MediatedCell-mediated rejectionCombination of cyclosporineT-cell infiltratesCell-dependent mechanismMononuclear cell infiltrateNatural killer cellsMononuclear cell infiltrationBlood mononuclear cellsSkin graft modelHuman immune responseImmunoglobulin G antibodiesMycosis Fungoides Palmaris et Plantaris or Acral Pagetoid Reticulosis?
McNiff J, Schechner J, Crotty P, Glusac E. Mycosis Fungoides Palmaris et Plantaris or Acral Pagetoid Reticulosis? American Journal Of Dermatopathology 1998, 20: 271-275. PMID: 9650701, DOI: 10.1097/00000372-199806000-00009.Peer-Reviewed Original ResearchConceptsMycosis fungoides palmaris et plantarisWoringer-Kolopp diseasePalmaris et plantarisPagetoid reticulosisEpidermotropic atypical lymphocytesPolymerase chain reaction studiesT-cell receptor betaT-cell clonalityClonal gene rearrangementsEpidermotropic lymphocytesRecurrent plaquesAtypical lymphocytesCutaneous plaquesSuppressor/Dermal infiltrateMycosis fungoidesSystemic diseaseAcral sitesT cellsBiologic potentialHistologic resemblanceIntraepidermal lymphocytesReceptor betaDiseasePlantarisExpression of integrin α4β7 on epidermotropic cutaneous T cells in cutaneous T cell lymphoma and spongiotic dermatitis
Schechner J, Edelson R, McNiff J, Heald P, Pober J. Expression of integrin α4β7 on epidermotropic cutaneous T cells in cutaneous T cell lymphoma and spongiotic dermatitis. Journal Of Dermatological Science 1998, 16: s168. DOI: 10.1016/s0923-1811(98)84004-8.Peer-Reviewed Original Research