0000000000380245

AUTHOR

Michael Lohoff

showing 10 related works from this author

Guidelines for the use of flow cytometry and cell sorting in immunological studies (second edition)

2019

All authors: Andrea Cossarizza Hyun‐Dong Chang Andreas Radbruch Andreas Acs Dieter Adam Sabine Adam‐Klages William W. Agace Nima Aghaeepour Mübeccel Akdis Matthieu Allez Larissa Nogueira Almeida Giorgia Alvisi Graham Anderson Immanuel Andrä Francesco Annunziato Achille Anselmo Petra Bacher Cosima T. Baldari Sudipto Bari Vincenzo Barnaba Joana Barros‐Martins Luca Battistini Wolfgang Bauer Sabine Baumgart Nicole Baumgarth Dirk Baumjohann Bianka Baying Mary Bebawy Burkhard Becher Wolfgang Beisker Vladimir Benes Rudi Beyaert Alfonso Blanco Dominic A. Boardman Christian Bogdan Jessica G. Borger Giovanna Borsellino Philip E. Boulais Jolene A. Bradford Dirk Brenner Ryan R. Brinkman Anna E. S. Broo…

0301 basic medicineConsensusImmunologyConsensuCell SeparationBiologyArticleFlow cytometry03 medical and health sciences0302 clinical medicineGuidelines ; Immunology ; Flow cytometryAllergy and ImmunologymedicineCell separationImmunology and AllergyHumansguidelines; flow cytometry; immunologymedicine.diagnostic_testBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.Cell sortingFlow CytometryCell selectionData science3. Good health030104 developmental biologyPhenotypeAllergy and Immunology; Cell Separation; Consensus; Flow Cytometry; Humans; Phenotype[SDV.IMM]Life Sciences [q-bio]/ImmunologyBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.030215 immunologyHumanEuropean journal of immunology
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Deep phenotypical characterization of human CD3\(^{+}\)CD56\(^{+}\) T cells by mass cytometry

2020

CD56\(^{+}\) T cells are a group of pro‐inflammatory CD3\(^{+}\) lymphocytes with characteristics of natural killer cells, being involved in antimicrobial immune defense. Here, we performed deep phenotypic profiling of CD3\(^{+}\)CD56\(^{+}\) cells in peripheral blood of normal human donors and individuals sensitized to birch‐pollen or/and house dust mite by high‐dimensional mass cytometry combined with manual and computational data analysis. A co‐regulation between major conventional T‐cell subsets and their respective CD3\(^{+}\)CD56\(^{+}\) cell counterparts appeared restricted to CD8\(^{+}\), MAIT, and TCRγδ\(^{+}\) T‐cell compartments. Interestingly, we find a co‐regulation of several …

0301 basic medicineCell specificImmune defenseCD3ImmunologyBiologyPhenotypeMolecular biologyPeripheral blood03 medical and health sciences030104 developmental biology0302 clinical medicineT cell subsetbiology.proteinImmunology and AllergyMass cytometryddc:610CD8030215 immunology
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The transcription factor IFN regulatory factor–4 controls experimental colitis in mice via T cell–derived IL-6

2008

The proinflammatory cytokine IL-6 seems to have an important role in the intestinal inflammation that characterizes inflammatory bowel diseases (IBDs) such as Crohn disease and ulcerative colitis. However, little is known about the molecular mechanisms regulating IL-6 production in IBD. Here, we assessed the role of the transcriptional regulator IFN regulatory factor-4 (IRF4) in this process. Patients with either Crohn disease or ulcerative colitis exhibited increased IRF4 expression in lamina propria CD3+ T cells as compared with control patients. Consistent with IRF4 having a regulatory function in T cells, in a mouse model of IBD whereby colitis is induced in RAG-deficient mice by transp…

AdultCD4-Positive T-LymphocytesMaleAdoptive cell transferRecombinant Fusion ProteinsT-LymphocytesCD3T cellAdoptive Transfer; Adult; Animals; Apoptosis; CD4-Positive T-Lymphocytes; Colitis; Cytokines; DNA-Binding Proteins; Female; Gene Expression Regulation; Humans; Inflammatory Bowel Diseases; Interferon Regulatory Factors; Interleukin-6; Intestinal Mucosa; Male; Mice; Mice Inbred C57BL; Mice Knockout; Middle Aged; Oxazolone; Receptors Interleukin-6; Recombinant Fusion Proteins; T-Lymphocytes; Trinitrobenzenesulfonic AcidApoptosisProinflammatory cytokineMiceIntestinal mucosamedicineAnimalsHumansIntestinal MucosaColitisInterleukin 6Mice KnockoutbiologyInterleukin-6OxazoloneGeneral MedicineMiddle AgedColitisInflammatory Bowel Diseasesmedicine.diseaseAdoptive TransferReceptors Interleukin-6Ulcerative colitisDNA-Binding ProteinsMice Inbred C57BLmedicine.anatomical_structureGene Expression RegulationTrinitrobenzenesulfonic AcidInterferon Regulatory FactorsImmunologybiology.proteinCytokinesFemaleResearch ArticleJournal of Clinical Investigation
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IRF4 regulates IL-17A promoter activity and controls RORγt-dependent Th17 colitis in vivo

2011

The transcription factor IRF4 is involved in several T-cell-dependent chronic inflammatory diseases. To elucidate the mechanisms for pathological cytokine production in colitis, we addressed the role of the IRF transcription factors in human inflammatory bowel disease (IBD) and experimental colitis.IRF levels and cytokine production in IBD patients were studied as well as the effects of IRF4 deficiency in experimental colitis.In contrast to IRF1, IRF5, and IRF8, IRF4 expression in IBD was augmented in the presence of active inflammation. Furthermore, IRF4 levels significantly correlated with IL-6 and IL-17 mRNA expression and to a lesser extent with IL-22 mRNA expression in IBD. To further …

AdultMaleElectrophoretic Mobility Shift AssayInflammatory bowel diseasePolymerase Chain Reaction03 medical and health sciencesMice0302 clinical medicineCrohn DiseaseRAR-related orphan receptor gammaImmunology and AllergyMedicineAnimalsHumansColitisInterleukin 6Promoter Regions GeneticTranscription factor030304 developmental biology0303 health sciencesCrohn's diseasebiologybusiness.industryInterleukin-6Interleukin-17GastroenterologyMiddle AgedNuclear Receptor Subfamily 1 Group F Member 3medicine.diseaseColitisInflammatory Bowel Diseasesdigestive system diseases3. Good health030220 oncology & carcinogenesisImmunologyInterferon Regulatory Factorsbiology.proteinTh17 CellsColitis UlcerativeFemaleInterleukin 17businessInterferon regulatory factors
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Deficiency in the Transcription Factor Interferon Regulatory Factor (Irf)-2 Leads to Severely Compromised Development of Natural Killer and T Helper …

2000

Interferon (IFN) regulatory factor (IRF)-2 was originally described as an antagonist of IRF-1–mediated transcriptional regulation of IFN-inducible genes. IRF-1−/− mice exhibit defective T helper type 1 (Th1) cell differentiation. We have used experimental leishmaniasis to show that, like IRF-1−/− mice, IRF-2−/− mice are susceptible to Leishmania major infection due to a defect in Th1 differentiation. Natural killer (NK) cell development is compromised in both IRF-1−/− and IRF-2−/− mice, but the underlying mechanism differs. NK (but not NK+ T) cell numbers are decreased in IRF-2−/− mice, and the NK cells that are present are immature in phenotype. Therefore, like IRF-1, IRF-2 is required for…

CD4-Positive T-LymphocytesMaleInterferon Regulatory Factor 2Cellular differentiationImmunologyLeishmaniasis CutaneousBiologyNitric OxideTh1MiceInterleukin 21Immune systemBone MarrowInterferonmedicineAnimalsImmunology and AllergyLymphocyte CountLeishmania majorInterleukin-15Mice KnockoutLeishmaniaMice Inbred BALB Cnatural killer cellsCell DifferentiationTh1 CellsInterleukin-12Cell biologyDNA-Binding ProteinsKiller Cells NaturalMice Inbred C57BLRepressor ProteinsDisease Models AnimalInterleukin 15interferon regulatory factorImmunologyInterleukin 12FemaleOriginal ArticleDisease SusceptibilityInterferon Regulatory Factor-2interleukin 15Transcription FactorsInterferon regulatory factorsmedicine.drugJournal of Experimental Medicine
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Different response of TH1 cells for stimulation with anti-CD3 antibodies.

1990

In this report, evidence is provided for a further subdivision of CD4+ T helper cell lines. The earlier definition of the TH1 and TH2 subtypes was confirmed by their differential response to interleukin (IL) 1. An additional subdivision of the TH1 subset was revealed when TH1 cell lines were costimulated with anti-CD3 antibodies and IL2. The IL2-induced proliferation of three of the resulting TH1 lines was blocked by anti-CD3 antibodies. By contrast, no such block was observed in a fourth TH1 cell line. In all four lines anti-CD3 triggering caused production of IL2. The block of proliferation was reversed neither by antigen-presenting cells nor by phorbol 12-myristate 13-acetate, a protein …

Antigens Differentiation T-LymphocyteCD4-Positive T-LymphocytesCD3 ComplexCell Survivalmedicine.medical_treatmentImmunologyDose-Response Relationship ImmunologicReceptors Antigen T-CellMice Inbred StrainsBiologyLymphocyte Activationchemistry.chemical_compoundMiceAntigenmedicineImmunology and AllergyAnimalsInterleukin 4Cell growthInterleukinAntibodies MonoclonalT helper cellT-Lymphocytes Helper-InducerMolecular biologyCytokinemedicine.anatomical_structurechemistryCell cultureImmunologyPhorbolInterleukin-2Tetradecanoylphorbol AcetateInterleukin-4SpleenEuropean journal of immunology
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Guidelines for the use of flow cytometry and cell sorting in immunological studies

2017

The marriage between immunology and cytometry is one of the most stable and productive in the recent history of science. A rapid search in PubMed shows that, as of July 2017, using “flow cytometry immunology” as a search term yields more than 68 000 articles, the first of which, interestingly, is not about lymphocytes. It might be stated that, after a short engagement, the exchange of the wedding rings between immunology and cytometry officially occurred when the idea to link fluorochromes to monoclonal antibodies came about. After this, recognizing different types of cells became relatively easy and feasible not only by using a simple fluorescence microscope, but also by a complex and some…

0301 basic medicineT-LymphocytesCell SeparationT cell precursors0302 clinical medicineImmunophenotypingHuman lymphopoiesis[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyImmunology and AllergyNon-U.S. Gov'tImmunologic Techniquemedicine.diagnostic_testResearch Support Non-U.S. Gov'tvirus diseaseshemic and immune systemsFalse Positive ReactionCell sortingFlow Cytometrynatural killer and innate lymphoid cells differentiation3. Good healthResearch Design[SDV.IMM]Life Sciences [q-bio]/ImmunologyHumanQuality Controlmedicine.drug_classImmunologyAnimals; Cell Proliferation; Cell Separation; DNA; False Positive Reactions; Flow Cytometry; Humans; Immunophenotyping; Quality Control; RNA; Research Design; Software; T-Lymphocytes; Guidelines as Topic; Immunologic Techniques; Immunology and Allergy; Immunologychemical and pharmacologic phenomenaGuidelines as TopicComputational biologyBiologyMonoclonal antibodyResearch SupportArticleFlow cytometryImmunophenotypingN.I.H.03 medical and health sciencesImmune systemImmunologic TechniqueResearch Support N.I.H. Extramuralmedicineearly lymphoid progenitorsJournal ArticleAnimalsHumansMass cytometryFalse Positive ReactionsImmunology and Allergy; Immunology; Flow cytometryIMUNOLOGIACell ProliferationAnimalExtramuralB cell ontogenyDNA030104 developmental biologyT-LymphocyteImmunologic TechniquesRNACytometrySoftware030215 immunologyEuropean Journal of Immunology
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Reciprocal regulation of the Il9 locus by counteracting activities of transcription factors IRF1 and IRF4.

2017

The T helper 9 (Th9) cell transcriptional network is formed by an equilibrium of signals induced by cytokines and antigen presentation. Here we show that, within this network, two interferon regulatory factors (IRF), IRF1 and IRF4, display opposing effects on Th9 differentiation. IRF4 dose-dependently promotes, whereas IRF1 inhibits, IL-9 production. Likewise, IRF1 inhibits IL-9 production by human Th9 cells. IRF1 counteracts IRF4-driven Il9 promoter activity, and IRF1 and IRF4 have opposing function on activating histone modifications, thus modulating RNA polymerase II recruitment. IRF1 occupancy correlates with decreased IRF4 abundance, suggesting an IRF1-IRF4-binding competition at the I…

0301 basic medicineCD4-Positive T-LymphocytesScienceCellular differentiationAntigen presentationGeneral Physics and AstronomyRNA polymerase IIMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciences0302 clinical medicineInterferonmedicineAnimalsHumansInterleukin 9Transcription factorMice KnockoutMultidisciplinaryGene Expression ProfilingQInterleukin-9Cell DifferentiationGeneral ChemistryT-Lymphocytes Helper-InducerCell biologyMice Inbred C57BL030104 developmental biologyIRF1Interferon Regulatory Factorsbiology.protein030215 immunologyInterferon regulatory factorsmedicine.drugInterferon Regulatory Factor-1Nature communications
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Tick Salivary Sialostatin L Represses the Initiation of Immune Responses by Targeting IRF4-Dependent Transcription in Murine Mast Cells

2015

Abstract Coevolution of ticks and the vertebrate immune system has led to the development of immunosuppressive molecules that prevent immediate response of skin-resident immune cells to quickly fend off the parasite. In this article, we demonstrate that the tick-derived immunosuppressor sialostatin L restrains IL-9 production by mast cells, whereas degranulation and IL-6 expression are both unaffected. In addition, the expression of IL-1β and IRF4 is strongly reduced in the presence of sialostatin L. Correspondingly, IRF4- or IL-1R–deficient mast cells exhibit a strong impairment in IL-9 production, demonstrating the importance of IRF4 and IL-1 in the regulation of the Il9 locus in mast cel…

Transcription GeneticCell DegranulationInterleukin-1betaImmunologyBiologyArticleCell DegranulationHost-Parasite InteractionsMiceImmune systemImmunityAnimalsImmunology and AllergyInterleukin 9Mast CellsPromoter Regions GeneticMice KnockoutRegulation of gene expressionMice Inbred BALB CBinding SitesInterleukin-6Interleukin-9DegranulationReceptors Interleukin-1CystatinsAsthmaImmunity InnateMice Inbred C57BLGene Expression RegulationInterferon Regulatory FactorsImmunologySignal transductionImmunosuppressive AgentsProtein BindingSignal TransductionInterferon regulatory factors
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Interferon-regulatory factor 4 is essential for the developmental program of T helper 9 cells.

2010

Summary Interferon-regulatory factor 4 (IRF4) is essential for the development of T helper 2 (Th2) and Th17 cells. Herein, we report that IRF4 is also crucial for the development and function of an interleukin-9 (IL-9)-producing CD4 + T cell subset designated Th9. IRF4-deficient CD4 + T cells failed to develop into IL-9-producing Th9 cells, and IRF4-specific siRNA inhibited IL-9 production in wild-type CD4 + T cells. Chromatin-immunoprecipitation (ChIP) analyses revealed direct IRF4 binding to the Il9 promoter in Th9 cells. In a Th9-dependent asthma model, neutralization of IL-9 substantially ameliorated asthma symptoms. The relevance of these findings is emphasized by the fact that the ind…

ImmunologyBiologyPathogenesisInterleukin 21MiceDownregulation and upregulationmedicineImmunology and AllergyAnimalsHumansInterleukin 9RNA Small InterferingMOLIMMUNOPromoter Regions GeneticCells CulturedMice KnockoutInterleukin-9Cell DifferentiationT helper cellT-Lymphocytes Helper-InducerAsthmaMice Inbred C57BLInfectious Diseasesmedicine.anatomical_structureCELLIMMUNOImmunologyInterferon Regulatory FactorsFunction (biology)Platelet factor 4IRF4Protein BindingImmunity
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