Search results for "Interferon type I"

showing 10 items of 39 documents

Donor interleukin-22 and host type I interferon signaling pathway participate in intestinal graft-versus-host disease via STAT1 activation and CXCL10.

2014

Acute graft-versus-host disease (aGVHD) remains a major complication following allogeneic hematopoietic cell transplantation, limiting the success of this therapy. We previously reported that interleukin-22 (IL-22) participates to aGVHD development, but the underlying mechanisms of its contribution remain poorly understood. In this study, we analyzed the mechanism of the pathological function of IL-22 in intestinal aGVHD. Ex-vivo colon culture experiments indicated that IL-22 was able to induce Th1-like inflammation via signal transducer and activator of transcription factor-1 (STAT1) and CXCL10 induction in the presence of type I interferon (IFN). To evaluate a potential synergy between IL…

0301 basic medicineImmunologyGraft vs Host DiseaseInflammationReceptor Interferon alpha-betaInterleukin 2203 medical and health sciencesMiceInterferonimmune system diseasesBone MarrowmedicineImmunology and AllergyCXCL10AnimalsTransplantation HomologousHumansSTAT1Intestine LargeIntestinal MucosaBone Marrow TransplantationMice KnockoutMice Inbred BALB CbiologyInterleukinsTh1 CellsTissue DonorsTransplantationMice Inbred C57BLChemokine CXCL10030104 developmental biologymedicine.anatomical_structuresurgical procedures operativeSTAT1 Transcription FactorGene Expression RegulationHematologic NeoplasmsImmunologyInterferon Type Ibiology.proteinSTAT proteinBone marrowmedicine.symptomWhole-Body Irradiationmedicine.drugSignal Transduction
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The murine cytomegalovirus M35 protein antagonizes type I IFN induction downstream of pattern recognition receptors by targeting NF-κB mediated trans…

2017

The type I interferon (IFN) response is imperative for the establishment of the early antiviral immune response. Here we report the identification of the first type I IFN antagonist encoded by murine cytomegalovirus (MCMV) that shuts down signaling following pattern recognition receptor (PRR) sensing. Screening of an MCMV open reading frame (ORF) library identified M35 as a novel and strong negative modulator of IFNβ promoter induction following activation of both RNA and DNA cytoplasmic PRR. Additionally, M35 inhibits the proinflammatory cytokine response downstream of Toll-like receptors (TLR). Using a series of luciferase-based reporters with specific transcription factor binding sites, …

0301 basic medicineMuromegalovirusPhysiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundMiceWhite Blood Cells0302 clinical medicineCell SignalingTranscription (biology)InterferonAnimal CellsImmune PhysiologyMedicine and Health SciencesMembrane Receptor SignalingBiology (General)Enzyme-Linked ImmunoassaysReceptorConnective Tissue CellsbiologyToll-Like ReceptorsPattern recognition receptorNF-kappa BImmune Receptor SignalingEnzymesThe murine cytomegalovirus M35 protein antagonizes type I IFN induction downstream of pattern recognition receptors by targeting NF-κB mediated transcription.Connective TissueReceptors Pattern RecognitionCytomegalovirus InfectionsInterferon Type ISignal transductionCellular TypesAnatomyBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.OxidoreductasesLuciferasemedicine.drugProtein BindingSignal TransductionResearch ArticleViral proteinQH301-705.5Immune CellsImmunologyResearch and Analysis MethodsTransfectionMicrobiology03 medical and health sciencesViral ProteinsMuromegalovirusVirologyGeneticsmedicineAnimalsImmunoassaysMolecular Biology TechniquesMolecular BiologyBlood CellsMacrophagesBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.Biology and Life SciencesProteinsNF-κBInterferon-betaCell BiologyRC581-607Fibroblastsbiology.organism_classificationMolecular biology030104 developmental biologyBiological TissuechemistryEnzymologyImmunologic TechniquesParasitologyInterferonsImmunologic diseases. AllergySpleen030215 immunology
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IRF8 Transcription Factor Controls Survival and Function of Terminally Differentiated Conventional and Plasmacytoid Dendritic Cells, Respectively

2016

International audience; Interferon regulatory factor-8 (IRF8) has been proposed to be essential for development of monocytes, plasmacytoid dendritic cells (pDCs) and type 1 conventional dendritic cells (cDC1s) and remains highly expressed in differentiated DCs. Transcription factors that are required to maintain the identity of terminally differentiated cells are designated `' terminal selectors.'' Using BM chimeras, conditional Irf8(fl/fl) mice and various promotors to target Cre recombinase to different stages of monocyte and DC development, we have identified IRF8 as a terminal selector of the cDC1 lineage controlling survival. In monocytes, IRF8 was necessary during early but not late d…

0301 basic medicineT-LymphocytesCellular differentiationImmunologyCre recombinasePlasmacytoid dendritic cellBiologyMonocytesMice03 medical and health sciences0302 clinical medicineInterferonmedicineAnimalsImmunology and AllergyPromoter Regions GeneticMonocyteCell DifferentiationDendritic CellsDendritic cellCell biologyMice Inbred C57BL030104 developmental biologyInfectious Diseasesmedicine.anatomical_structureInterferon Regulatory FactorsInterferon Type ICancer research[SDV.IMM]Life Sciences [q-bio]/ImmunologyIRF8Transcription Factors030215 immunologyIRF4medicine.drugImmunity
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Treatment of Patients with Chronic Type B Hepatitis and Concurrent Human Immunodeficiency Virus Infection with a Combination of Interferon Alpha and …

1989

Six patients with chronic type B hepatitis and concurrent infection with the immunodeficiency virus were treated with 600 mg azidothymidine (AZT)/day and 3 X 10(6) units of interferon-alpha (IFN-alpha) every other day for a total of 4 months. None of the patients treated lost the hepatitis B virus (HBV). HBV-DNA concentrations were not significantly influenced by this treatment. Human immunodeficiency virus (HIV) infection was also not affected except for a transient rise in CD 4-positive cells in 2 individuals, who had initially low CD 4-positive cells. Treatment did not influence the presence of HIV-Ag in the serum. In conclusion, a combination therapy of IFN and AZT does not seem to be b…

AdultCD4-Positive T-LymphocytesMaleHepatitis B virusCombination therapyHIV AntigensAlpha interferonHIV InfectionsPilot Projectsmedicine.disease_causeLeukocyte CountZidovudineAcquired immunodeficiency syndrome (AIDS)InterferonHumansMedicineHepatitisHepatitis B virusbusiness.industryGastroenterologyvirus diseasesMiddle AgedHepatitis Bmedicine.diseaseVirologyDNA ViralInterferon Type IImmunologyDrug Therapy CombinationFemaleViral diseasebusinessZidovudinemedicine.drugDigestion
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Type I interferons as the potential mechanism linking mRNA COVID-19 vaccines to Bell's palsy

2021

Therapies - Sous presse. Epreuves corrigees par l'auteur. Disponible en ligne depuis le mardi 13 avril 2021

AdultMale2019-20 coronavirus outbreakCoronavirus disease 2019 (COVID-19)Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)COVID-19 vaccines030226 pharmacology & pharmacyArticle03 medical and health sciencesPharmacovigilance0302 clinical medicineBell's palsyPhase 3 clinical trialsBell PalsymedicineType I interferonsHumansBell's palsyPharmacology (medical)Potential mechanismComputingMilieux_MISCELLANEOUSAgedCOVID-19 coronavirus disease 2019Vaccines SyntheticMessenger RNASARS-CoV-2business.industryCOVID-19Bell’s palsyMiddle Agedmedicine.diseaseVirologymRNA messenger RNA3. Good healthInterferon Type IFemale[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologiebusiness
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Circulating E-selectin levels in chronic hepatitis C patients with normal or elevated transaminase before and after alpha-interferon treatment

2001

E-selectin, an adhesion molecule of the selectin family, is involved in leukocyte adhesion to the endothelium and in the cellular immunological reactions. Expression of this molecule, in fact, is physiologically absent, but it becomes evident on sinusoidal lining cells during inflammatory liver disease. The aim of this study was to evaluate the behavior of E-selectin in chronic hepatitis C (CH-C) patients with persistently normal transaminase in comparison to patients with CH-C and elevated transaminase, and its changes during alpha-interferon therapy. Immunohistochemical localization of E-selectin was also performed on liver tissue specimens of both groups. Fifty-eight subjects were divide…

AdultMaleAdhesion moleculeChronic liver diseaseE-selectinImmunologyAlanine TransaminaseHepatitis C ChronicMiddle AgedImmunohistochemistryRecombinant ProteinsTreatmentLiverInterferon Type IHumansα-interferonImmunology and AllergyFemaleAspartate Aminotransferases
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Treatment of 11 patients with chronic myelogenous leukemia with interferon-alpha-2C and low-dose cytosine arabinoside

1993

Abstract Patients with Philadelphia (Ph) chromosome-positive chronic myelogenous leukemia (CML) and on interferon (IFN)-α-2c treatment for at least two months were entered in the present pilot study. IFN-α treatment was maintained identically and cytosine arabinoside (Ara-C) was added at monthly cycles of 10 mg/m 2 /day for ten days subcutaneously. In the case of a leukocyte nadir above 10 G/1, the Ara-C dose was increased to 20 mg/m 2 /day for 10 days per month. Ten of the eleven patients entered in this study were evaluable for toxicity and response. They received a total of 87 IFN-α/Ara-C cycles (3–14/patient). Five patients received 1–5 cycles with Ara-C dose intensification to 20 mg/m …

AdultMaleCancer Researchmedicine.medical_specialtyNauseamedicine.medical_treatmentAlpha interferonGastroenterologyDrug Administration ScheduleLeukocyte CountLeukemia Myelogenous Chronic BCR-ABL PositiveInternal medicinemedicineHumansInterferon alfaAgedChemotherapybusiness.industryCytarabineHematologyMiddle Agedmedicine.diseaseCombined Modality TherapyRecombinant ProteinsSurgeryDiarrheaOncologyInterferon Type IToxicityCytarabineFemalemedicine.symptombusinessmedicine.drugChronic myelogenous leukemiaLeukemia Research
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The effect of recombinant alpha-interferon treatment on serum levels of hepatitis B virus-encoded proteins in man.

1987

The effect of alpha-interferon treatment on serum levels of hepatitis B virus-encoded proteins was analyzed in eight patients with chronic type B hepatitis who participated in a pilot study of interferon therapy. Three individuals became HBsAg-negative, 4 lost HBeAg but remained HBsAg-positive and 1 remained positive for both HBsAg and HBeAg. Initiation of interferon treatment was rapidly followed by reduction or loss of hepatitis B virus DNA in the serum but by little immediate change in hepatitis B virus antigen levels. Changes in hepatitis B virus antigens were usually delayed. Loss of HBsAg from the serum was preceded by the sequential disappearance of pre-S-encoded proteins (pre-S1 and…

AdultMaleHBsAgGenes ViralvirusesAlpha interferonmedicine.disease_causeHepatitis B AntigensViral ProteinsInterferonmedicineHumansHepatitis B e AntigensHepatitis ChronicHepatitis B virusHepatitisHepatitis B Surface AntigensHepatologybusiness.industryvirus diseasesHepatitis BMiddle Agedmedicine.diseaseHuman serum albuminVirologydigestive system diseasesRecombinant ProteinsHBeAgImmunologyDNA ViralInterferon Type IFemalebusinessmedicine.drugHepatology (Baltimore, Md.)
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Deficiency of the autoimmune regulator AIRE in thymomas is insufficient to elicit autoimmune polyendocrinopathy syndrome type 1 (APS‐1)

2007

Thymomas are thymic epithelial neoplasms, associated with a variety of autoimmune disorders (especially myasthenia gravis), that apparently result from aberrant intra-tumourous thymopoiesis and export of inefficiently tolerized T-cells to the periphery. The autoimmune regulator (AIRE) drives the expression of self-antigens in the thymic medulla and plays an essential role in ‘central’ tolerance in both humans and mice. However, while inactivating AIRE mutations result in the ‘autoimmune polyendocrinopathy syndrome type 1’ (APS-1), its major features are not well reproduced in AIRE-knock-out mice. Therefore, alternative human disease scenarios with concomitant AIRE deficiency may be valuable…

AdultMaleThymomaAdolescentThymomaAntibodies NeoplasmThymus Glandmedicine.disease_causeAutoantigensAutoimmune DiseasesPathology and Forensic MedicineAutoimmunity03 medical and health sciences0302 clinical medicineAntigens NeoplasmInterferonMyasthenia GravismedicineHumansPolyendocrinopathies AutoimmuneAgedAutoantibodies030304 developmental biologyAged 80 and over0303 health sciencesbiologybusiness.industryAutoantibodyThymus NeoplasmsMiddle AgedAutoimmune regulatormedicine.diseaseImmunohistochemistryMyasthenia gravisNeoplasm Proteins3. Good healthThymic Tissue030220 oncology & carcinogenesisInterferon Type IImmunologybiology.proteinCytokinesFemaleAntibodybusinessTranscription Factorsmedicine.drugThe Journal of Pathology
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Interferon alfa-2c in chronic myelogenous leukemia (CML): hematologic, cytogenetic and molecular-genetic response of patients with chronic phase CML …

1990

Alpha- and gamma-interferons have been shown to actively suppress hematopoiesis in patients in the chronic phase of chronic myelogenous leukemia in vitro and in vivo. Since both interferons act through different receptors on their hematopoietic target cells, they are expected to be capable of independently inhibiting abnormal blood cell development in patients with chronic myelogenous leukemia. We have utilized recombinant human interferon alfa-2c to treate 11 patients with Philadelphia chromosome positive chronic myelogenous leukemia in chronic phase, who were resistant to previous interferon gamma therapy. Ten of the patients were evaluable for hematologic, cytogenetic and molecular-genet…

AdultMalemedicine.medical_specialtyDrug ResistanceAlpha interferonBiologyCytogeneticsInterferon-gammaInterferonhemic and lymphatic diseasesInternal medicineLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansInterferon gammaInterferon alfaHematologybreakpoint cluster regionHematologyGeneral MedicineMiddle Agedmedicine.diseaseHematologic ResponseRecombinant ProteinsImmunologyInterferon Type ICancer researchDrug EvaluationFemalemedicine.drugChronic myelogenous leukemiaBlut
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