Search results for "immune system diseases"

showing 10 items of 442 documents

Abacavir Induces Arterial Thrombosis in a Murine Model.

2018

Background The purinergic system is known to underlie prothrombotic and proinflammatory vascular programs, making the profile of experimental actions demonstrated by abacavir compatible with thrombogenesis. However, direct evidence of a prothrombotic effect by the drug has been lacking. Methods The present study appraised the effects of abacavir in a well-validated animal model of arterial thrombosis. The role of ATP-P2X7 receptors in the actions of the drug was also assessed, and the actions of recognized vascular-damaging agents and other nucleoside reverse-transcriptase inhibitors (NRTIs) were evaluated and compared to those of abacavir. Results Abacavir dose-dependently promoted thrombu…

0301 basic medicineDrugMaleAnti-HIV Agentsmedia_common.quotation_subject030204 cardiovascular system & hematologyPharmacologyProinflammatory cytokine03 medical and health sciences0302 clinical medicineimmune system diseasesAbacavirmedicineImmunology and AllergyAnimalsRofecoxibmedia_commonMice KnockoutDose-Response Relationship Drugbusiness.industryPurinergic receptorAntagonistvirus diseasesThrombosisPurinergic signallingmedicine.diseaseThrombosisDideoxynucleosidesDisease Models Animal030104 developmental biologyInfectious DiseasesReceptors Purinergic P2X7businessmedicine.drugThe Journal of infectious diseases
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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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HSP110 sustains chronic NF-κB signaling in activated B cell diffuse large B cell lymphoma through MyD88 stabilization

2018

International audience; Activated B cell diffuse large B cell lymphoma (ABC-DLBCL) is an aggressive lymphoproliferative disorder involving chronic NF-κB activation. Several mutations in the BCR and the MyD88 signaling pathway components, such as MyD88 L265P, are implicated in this aberrant activation. Among heat-shock proteins, HSP110 has recently been identified as a pro- survival and/or proliferation factor in many cancers but its role in ABC-DLBCL survival mechanisms remained to be established. We observed that shRNA-mediated HSP110 silencing decreased the survival of several ABC-DLBCL cell lines, decreased IgM-MyD88 co-localization and subsequent NF-κB signaling. Conversely, over-expres…

0301 basic medicineImmunology[SDV.CAN]Life Sciences [q-bio]/CancerBiochemistry[ SDV.CAN ] Life Sciences [q-bio]/CancerCohort Studies03 medical and health sciencesimmune system diseaseshemic and lymphatic diseasesmedicineTumor Cells CulturedGene silencingHumansHSP110 Heat-Shock ProteinsB cellChemistryProtein StabilityWild typebreakpoint cluster regionNF-kappa BCell BiologyHematologymedicine.disease3. Good healthLymphoma030104 developmental biologymedicine.anatomical_structureCell cultureMyeloid Differentiation Factor 88Cancer researchLymphoma Large B-Cell DiffuseSignal transductionDiffuse large B-cell lymphomaSignal Transduction
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Exogenous TNFR2 activation protects from acute GvHD via host T reg cell expansion

2015

Activation of TNFR2 with a novel agonist expands T reg cells in vivo and protects allo-HCT recipients from acute GvHD while sparing antilymphoma and antiinfectious properties of transplanted donor T cells.

0301 basic medicineInterleukin 2medicine.medical_treatmentImmunologyGraft vs Host DiseaseMice Inbred Strainschemical and pharmacologic phenomenaHematopoietic stem cell transplantationBiologyT-Lymphocytes RegulatoryArticleMice03 medical and health sciencesInterleukin 21immune system diseaseshemic and lymphatic diseasesmedicineAnimalsReceptors Tumor Necrosis Factor Type IIImmunology and AllergyCytotoxic T cellddc:610Research Articlesintegumentary systemMyeloid-Derived Suppressor CellsHematopoietic Stem Cell TransplantationFOXP3hemic and immune systemsmedicine.diseaseLeukemiaddc:57030104 developmental biologysurgical procedures operativeAcute DiseaseImmunologyMyeloid-derived Suppressor CellInterleukin-2FemaleTumor necrosis factor receptor 2medicine.drug
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Bone marrow B lymphocytes in multiple myeloma and MGUS: Focus on distribution of naïve cells and memory subsets.

2016

Multiple myeloma (MM) is caused by proliferation of clonal plasma cells (cPCs) in bone marrow (BM), associated with numerical and functional defects in immune subsets. An impairment of B cell compartment is involved in onset/progression of the disease.By flow cytometry, we studied distribution of naïve/transitional (IgD(+)CD27(-)), memory unswitched (IgD(+)CD27(+)), memory switched (IgD(-)CD27(+)) and double negative (DN) (IgD(-)CD27(-)) B lymphocytes in BM of control subjects, and responding and relapsing patients.We observed an increased percentage of IgD(+)CD27(+) B cells in healthy controls vs responding patients (p0.05). Treated non complete responders exhibited an expanded DN compartm…

0301 basic medicineMaleCancer ResearchB-Lymphocyte Subsetschemical and pharmacologic phenomenaBone Marrow CellsImmunoglobulin DMonoclonal Gammopathy of Undetermined SignificanceFlow cytometry03 medical and health sciencesImmune systemstomatognathic systemimmune system diseaseshemic and lymphatic diseasesmedicineHumansB cellMultiple myelomaB-Lymphocyte SubsetsB cellB-Lymphocytesmedicine.diagnostic_testbiologyhemic and immune systemsHematologyImmunoglobulin Dmedicine.diseaseFlow CytometryTumor Necrosis Factor Receptor Superfamily Member 7030104 developmental biologymedicine.anatomical_structureOncologyCase-Control StudiesImmunologybiology.proteinMGUSFemaleBone marrowMultiple MyelomaMonoclonal gammopathy of undetermined significanceLeukemia research
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CD19 Isoforms Enabling Resistance to CART-19 Immunotherapy Are Expressed in B-ALL Patients at Initial Diagnosis.

2017

Supplemental Digital Content is available in the text.

0301 basic medicineMaleCancer Researchmedicine.medical_treatmentT-LymphocytesEpitopes T-LymphocyteT-Cell Antigen Receptor SpecificityImmunotherapy AdoptiveEpitopeCohort StudiesExon0302 clinical medicineimmune system diseasesImmunology and AllergyMedicineProtein IsoformsChildAged 80 and overbiologyCD19CART-19B-ALLMiddle AgedPrecursor Cell Lymphoblastic Leukemia-Lymphomaepitope-lossmedicine.anatomical_structureTreatment Outcome030220 oncology & carcinogenesisChild PreschoolComputingMethodologies_DOCUMENTANDTEXTPROCESSINGFemaleClone (B-cell biology)Gene isoformAdultAdolescentRecombinant Fusion ProteinsImmunologyAntigens CD19Receptors Antigen T-CellCancer VaccinesCD1903 medical and health sciencesYoung AdultAntigenHumansAgedPharmacologybusiness.industryInfant NewbornisoformsInfantImmunotherapy030104 developmental biologyImmunologybiology.proteinClinical StudyTumor EscapeBone marrowbusinessJournal of immunotherapy (Hagerstown, Md. : 1997)
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Renal tubular epithelial cell-derived BAFF expression mediates kidney damage and correlates with activity of proliferative lupus nephritis in mouse a…

2017

B-cell activating factor of the tumour necrosis factor family (BAFF) is a cytokine, mainly produced by hematopoietic cells (e.g. monocytes/macrophages, dendritic cells), indispensable for B-cell maturation. The BLISS studies have demonstrated that blocking BAFF by the human monoclonal antibody belimumab is a valuable therapeutic approach in patients with clinically and serologically active systemic lupus erythematosus (SLE). However, the defined sources of BAFF, which contributes to SLE, are still unclear. Recent findings show that BAFF expression is not restricted to myeloid cells. Since lupus nephritis is the main cause of morbidity and mortality for SLE patients, the aim of this study wa…

0301 basic medicineMalemedicine.medical_treatmentLupus nephritisAntibodies Monoclonal HumanizedKidneySeverity of Illness IndexPathogenesis03 medical and health sciencesMice0302 clinical medicinestomatognathic systemRheumatologyimmune system diseasesB-Cell Activating FactormedicineAnimalsHumansLupus Erythematosus Systemicskin and connective tissue diseasesB-cell activating factorAutocrine signallingRetrospective StudiesB-Lymphocytesbusiness.industryTumor Necrosis Factor-alphaEpithelial Cellsmedicine.diseaseBelimumabLupus Nephritisstomatognathic diseasesHaematopoiesis030104 developmental biologyCytokineReceptors Granulocyte-Macrophage Colony-Stimulating FactorImmunologyCytokinesTumor necrosis factor alphaFemaleKidney DiseasesbusinessImmunosuppressive Agents030215 immunologymedicine.drugLupus
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A 13 mer LNA-i-miR-221 Inhibitor Restores Drug Sensitivity in Melphalan-Refractory Multiple Myeloma Cells.

2016

Abstract Purpose: The onset of drug resistance is a major cause of treatment failure in multiple myeloma. Although increasing evidence is defining the role of miRNAs in mediating drug resistance, their potential activity as drug-sensitizing agents has not yet been investigated in multiple myeloma. Experimental Design: Here we studied the potential utility of miR-221/222 inhibition in sensitizing refractory multiple myeloma cells to melphalan. Results: miR-221/222 expression inversely correlated with melphalan sensitivity of multiple myeloma cells. Inhibition of miR-221/222 overcame melphalan resistance and triggered apoptosis of multiple myeloma cells in vitro, in the presence or absence of…

0301 basic medicineMelphalanCancer ResearchStromal cellApoptosisDrug resistancePharmacologyArticle03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinemyeloma microRNA mir-221 melphalanimmune system diseasesIn vivohemic and lymphatic diseasesCell Line TumorProto-Oncogene ProteinsmedicineAnimalsHumansMelphalanMultiple myelomaNOD miceCell Proliferationbusiness.industryCancermedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyOncologychemistryDrug Resistance Neoplasm030220 oncology & carcinogenesisGrowth inhibitionMultidrug Resistance-Associated ProteinsbusinessApoptosis Regulatory ProteinsMultiple Myelomamedicine.drugClinical cancer research : an official journal of the American Association for Cancer Research
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IL-34–Dependent Intrarenal and Systemic Mechanisms Promote Lupus Nephritis in MRL-Faslpr Mice

2019

Background In people with SLE and in the MRL- Fas lpr lupus mouse model, macrophages and autoantibodies are central to lupus nephritis. IL-34 mediates macrophage survival and proliferation, is expressed by tubular epithelial cells (TECs), and binds to the cFMS receptor on macrophages and to a newly identified second receptor, PTPRZ. Methods To investigate whether IL-34–dependent intrarenal and systemic mechanisms promote lupus nephritis, we compared lupus nephritis and systemic illness in MRL- Fas lpr mice expressing IL-34 and IL-34 knockout (KO) MRL- Fas lpr mice. We also assessed expression of IL-34 and the cFMS and PTPRZ receptors in patients with lupus nephritis. Results Intrarenal IL-3…

0301 basic medicineMice Inbred MRL lprChemokineCell SurvivalLupus nephritisRisk AssessmentMonocytesMice03 medical and health sciences0302 clinical medicineSpecies Specificityimmune system diseasesmedicineAnimalsMacrophageMolecular Targeted Therapyskin and connective tissue diseasesCells CulturedCell ProliferationMice KnockoutSystemic lupus erythematosusCell Deathbiologybusiness.industryInterleukinsMacrophagesGeneral MedicineMonocyte proliferationmedicine.diseaseLupus NephritisMice Inbred C57BLDisease Models AnimalBasic ResearchKidney Tubules030104 developmental biologyGene Expression RegulationNephrology030220 oncology & carcinogenesisImmunologyKnockout mouseDisease Progressionbiology.proteinChemokinesbusinessMacrophage proliferationNephritisJournal of the American Society of Nephrology
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Sex-dependent metabolism of nevirapine in rats: impact on plasma levels, pharmacokinetics and interaction with nortriptyline.

2017

Abstract Nevirapine (NVP) is a non-nucleoside reverse transcriptase inhibitor (NNRTI) widely used in the treatment of human immunodeficiency virus type 1 (HIV-1) and is the first-choice NNRTI during pregnancy. NVP shows a sex dimorphic profile in humans with sex differences in bioavailability, biotransformation and toxicity. In this study, sex differences in NVP metabolism and inhibition of NVP metabolism by the antidepressant nortriptyline (NT) were evaluated using rats as experimental animals. NVP was administered orally to male and female rats and sex differences in plasma levels and pharmacokinetic parameters were analysed. NVP plasma levels were higher in female compared with male rats…

0301 basic medicineMicrobiology (medical)Malemedicine.medical_specialtyNevirapineMetabolite030106 microbiologyCmaxNortriptylineAntidepressive Agents Tricyclic030226 pharmacology & pharmacy03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSex FactorsPharmacokineticsimmune system diseasesInternal medicinemedicineAnimalsPharmacology (medical)Drug InteractionsNevirapineRats WistarIC50Chemistryvirus diseasesGeneral MedicineBioavailabilityInfectious DiseasesEndocrinologyToxicityMicrosomes LiverReverse Transcriptase InhibitorsFemaleNortriptylinemedicine.drugInternational journal of antimicrobial agents
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