Search results for "D4 [Ratio D2]"

showing 10 items of 59 documents

Protection from graft-versus-host disease by HIV-1 envelope protein gp120-mediated activation of human CD4+CD25+ regulatory T cells.

2009

AbstractNaturally occurring CD4+CD25+ regulatory T cells (Tregs) represent a unique T-cell lineage that is endowed with the ability to actively suppress immune responses. Therefore, approaches to modulate Treg function in vivo could provide ways to enhance or reduce immune responses and lead to novel therapies. Here we show that the CD4 binding human immunodeficiency virus-1 envelope glycoprotein gp120 is a useful and potent tool for functional activation of human Tregs in vitro and in vivo. Gp120 activates human Tregs by binding and signaling through CD4. Upon stimulation with gp120, human Tregs accumulate cyclic adenosine monophosphate (cAMP) in their cytosol. Inhibition of endogeneous cA…

ImmunologyTransplantation HeterologousGraft vs Host Diseasechemical and pharmacologic phenomenaCHO CellsMice SCIDBiologyHIV Envelope Protein gp120Lymphocyte ActivationBiochemistryT-Lymphocytes RegulatoryImmune tolerancechemistry.chemical_compoundMiceImmune systemCricetulusIn vivoMice Inbred NODCricetinaeCyclic AMPImmune ToleranceAnimalsHumansCyclic adenosine monophosphateIL-2 receptorhemic and immune systemsCell BiologyHematologyEnvelope glycoprotein GP120Cell biologyTransplantationchemistryImmunologyCD4 Antigensbiology.proteinHIV-1Signal transductionSignal TransductionBlood
researchProduct

Etude de la régulation transcriptionnelle des lymphocytes T CD4 dans un contexte de cancer : application en immunothérapie anticancéreuse

2015

Immune surveillance of tumors is based on the ability of effector cells of the immune system to detect and eliminate the cancer cells. Notwithstanding, the complete and spontaneous regression of established cancers was observed only in very few cases. The failure of cancer resolution by the immune system could result from the combination of several factors: i) inadequate immune response related to a low tumor immunogenicity, ii) incompetent immune system consecutively to induced or acquired immunodeficiencies and iii) the selection of resistant tumor variants able to thwart immune surveillance or subverting immune responses. Developing novel cancer immunotherapy strategies leading to potent…

Immunothérapie anticancéreuse[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyRégulation transcriptionnelleCancer immunotherapyIRF1CD4 T cell differentiationDifférenciation lymphocytaire T CD4DHAIFR1Transcriptional regulation[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathology[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
researchProduct

Distinct Roles for IL-1 Receptor Type I Signaling in Early Versus Established Leishmania major Infections

2006

IL-1alpha/beta released by infected dendritic cells (DC) plays a critical role in the development of protective immunity against Leishmania major. Previous studies demonstrated that treatment of susceptible BALB/c mice with IL-1alpha during T-cell priming (days 1-3 post-infection) induced T helper (Th)1-mediated protection. In contrast, we now demonstrate that prolonged treatment with IL-1alpha (for 3 weeks) worsened disease outcome. To characterize the receptor involved, L. major infections in IL-1 receptor type I (IL-1RI) knockout mice were studied. In C57BL/6 IL-1RI-/- mice, the IL-1alpha-mediated protective effect was abrogated. The course of high-dose infection (2 x 10(5) parasites) in…

Leishmaniasis CutaneousPriming (immunology)DermatologyReceptor typeBiochemistryInterferon-gammaMiceTh2 CellsmedicineAnimalsParasite hostingLeishmania majorL-SelectinReceptorMolecular BiologyLeishmania majorMice KnockoutReceptors Interleukin-1 Type IMice Inbred BALB CbiologyReceptors Interleukin-1LeishmaniasisT-Lymphocytes Helper-InducerCell BiologyTh1 Cellsbiology.organism_classificationmedicine.diseaseMice Inbred C57BLGene Expression RegulationCD4 AntigensImmunologyKnockout mouseDisease ProgressionInterleukin-4Ex vivoInterleukin-1Signal TransductionJournal of Investigative Dermatology
researchProduct

Serum leptin and interleukin-6 levels in pediatric patients with HIV.

2003

Recent therapeutic approaches have improved the prognosis of children with HIV. Many new efforts could be involved in their quality of life and therefore could need additional diagnostic strategies. Leptin regulates pubertal development; furthermore a continuous immune stimulus, as in chronic infectious diseases, can enhance leptin's secretion by the action of cytokines such as interleukin (IL)-6. To clarify this role in patients infected with HIV, we assayed leptin and IL-6 and evaluated the influence of HIV severity on its secretion. IL-6 (380.5 +/- 257.6 pg/ml; range: 22-900 pg/ml) showed a significant correlation with leptinemia, HIV-1 RNA, and viremia related to the stage of HIV diseas…

LeptinMalemedicine.medical_specialtyAnti-HIV AgentsEndocrinology Diabetes and MetabolismViremiaEnzyme-Linked Immunosorbent AssayHIV InfectionsPubertal stageEndocrinologyImmune systemStatistical significanceInternal medicinemedicineHumansHIV InfectionSecretionSexual MaturationInterleukin 6ChildPediatric HIVbiologybusiness.industryInterleukin-6Reverse Transcriptase Polymerase Chain ReactionCD4 AntigenLeptinPubertyAnti-HIV AgentInterleukinInfantmedicine.diseaseEndocrinologyChild PreschoolPediatrics Perinatology and Child HealthImmunologyCD4 Antigensbiology.proteinHIV-1Receptors LeptinFemalebusinessHumanJournal of pediatric endocrinologymetabolism : JPEM
researchProduct

P38 MAP Kinase Signaling Is Required for the Conversion of CD4+CD25− T Cells into iTreg

2008

CD4+CD25+ regulatory T cells (Treg) are important mediators of immune tolerance. A subset of Treg can be generated in the periphery by TGF-beta dependent conversion of conventional CD4+CD25− T cells into induced Treg (iTreg). In chronic viral infection or malignancy, such induced iTreg, which limit the depletion of aberrant or infected cells, may be of pathogenic relevance. To identify potential targets for therapeutic intervention, we investigated the TGF-beta signaling in Treg. In contrast to conventional CD4+ T cells, Treg exhibited marked activation of the p38 MAP kinase pathway. Inhibition of p38 MAP kinase activity prevented the TGF-beta-dependent conversion of CD4+CD25− T cells into …

MAPK/ERK pathwayp38 mitogen-activated protein kinasesImmunologyBlotting WesternImmunology/Immunomodulationlcsh:MedicineImmunology/Autoimmunitychemical and pharmacologic phenomenaBiologyT-Lymphocytes Regulatoryp38 Mitogen-Activated Protein KinasesImmune toleranceImmunology/Leukocyte Signaling and Gene ExpressionMiceAnimalsIL-2 receptorlcsh:ScienceMultidisciplinarylcsh:RInterleukin-2 Receptor alpha SubunitFOXP3hemic and immune systemsFlow CytometryCell biologyMitogen-activated protein kinaseCD4 Antigensbiology.proteinPhosphorylationlcsh:QSignal transductionResearch ArticleSignal TransductionPLoS ONE
researchProduct

Local increase of arginase activity in lesions of patients with cutaneous leishmaniasis in Ethiopia.

2012

Background Cutaneous leishmaniasis is a vector-borne disease that is in Ethiopia mainly caused by the parasite Leishmania aethiopica. This neglected tropical disease is common in rural areas and causes serious morbidity. Persistent nonhealing cutaneous leishmaniasis has been associated with poor T cell mediated responses; however, the underlying mechanisms are not well understood. Methodology/Principal Findings We have recently shown in an experimental model of cutaneous leishmaniasis that arginase-induced L-arginine metabolism suppresses antigen-specific T cell responses at the site of pathology, but not in the periphery. To test whether these results translate to human disease, we recruit…

MalePathologyCD3 ComplexBiopsyAntigens CD8Antigens CD3Antigens CD40302 clinical medicineINFECTIONSUPPRESSOR-CELLSAETHIOPICAChildImmune ResponseSOUTH-WESTERN ETHIOPIAIN-VIVOSkin0303 health sciencesbiologyPARASITOLOGYlcsh:Public aspects of medicine11 Medical And Health SciencesMiddle Aged3. Good healthArginaseInfectious Diseasesmedicine.anatomical_structureCD4 AntigensMedicineFemalemedicine.symptomLife Sciences & BiomedicineResearch ArticleNeglected Tropical DiseasesEXPRESSIONAdultmedicine.medical_specialtylcsh:Arctic medicine. Tropical medicineAdolescentlcsh:RC955-962CD8 AntigensT cellImmunology030231 tropical medicineLeishmaniasis CutaneousPeripheral blood mononuclear cellImmunomodulationLesionYoung Adult03 medical and health sciencesLeishmania aethiopicaCutaneous leishmaniasisTropical MedicineParasitic DiseasesL-ARGININE METABOLISMmedicineACTIVATED GRANULOCYTESHumansBiology030304 developmental biologyScience & TechnologyNITRIC-OXIDEArginasebusiness.industryPublic Health Environmental and Occupational HealthLeishmaniasislcsh:RA1-127006 Biological Sciencesbiology.organism_classificationmedicine.diseaseMICEImmunologyLeukocytes MononuclearEthiopiabusinessCD8PLoS Neglected Tropical Diseases
researchProduct

Trimeric HIV Env provides epitope occlusion mediated by hypervariable loops

2014

AbstractHypervariable loops of HIV-1 Env protein gp120 are speculated to play roles in the conformational transition of Env to the receptor binding-induced metastable state. Structural analysis of full-length Env-based immunogens, containing the entire V2 loop, displayed tighter association between gp120 subunits, resulting in a smaller trimeric diameter than constructs lacking V2. A prominent basal quaternary location of V2 and V3′ that challenges previous reports would facilitate gp41-independent gp120-gp120 interactions and suggests a quaternary mechanism of epitope occlusion facilitated by hypervariable loops. Deletion of V2 resulted in dramatic exposure of basal, membrane-proximal gp41…

Models MolecularProtein ConformationvirusesHuman immunodeficiency virus (HIV)[CHIM.THER]Chemical Sciences/Medicinal ChemistryPlasma protein bindingHIV Envelope Protein gp120medicine.disease_causeEnv ProteinEpitopeenv Gene ProductsEpitopesProtein structureModelsComputingMilieux_MISCELLANEOUSSequence DeletionGeneticsMultidisciplinary[SDV.BBM.BS]Life Sciences [q-bio]/Biochemistry Molecular Biology/Structural Biology [q-bio.BM]Transition (genetics)biologyenv Gene Products Human Immunodeficiency Virusvirus diseaseshypervariable loopsHIV Envelope Protein gp41[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]3. Good health[SDV.BBM.BS]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]CD4 AntigensHIV/AIDSAntibodyHuman Immunodeficiency VirusProtein BindingEnvGp41ArticleVaccine RelatedGenetics[CHIM.CRIS]Chemical Sciences/CristallographymedicineHumansProtein Interaction Domains and Motifs[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]AntigensVaccine Related (AIDS)Preventionta1182Molecular[SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/ImmunotherapyCD4Peptide Fragmentsgp120Good Health and Well BeingHIV-1biology.proteinImmunizationProtein MultimerizationproteinScientific Reports
researchProduct

Human immunodeficiency virus infection in cells of myeloid-monocytic lineage.

1991

We established persistent infection with a strain of human immunodeficiency virus type 1, HTLV-IIIB, in a promyelomonocytic cell line, ML-1 (CD4 antigen nearly negative and CD4 mRNA negative), and a promonocytic cell line, THP-1 (CD4 antigen positive). Different reaction of giant cell formation was found after co-cultivation of infected and uninfected cells of ML-1, HL-60, THP-1 and U-937 cell lines with uninfected and infected MOLT4 (a T-lymphoma cell line).

MyeloidVirus CultivationCD4 antigenImmunologyFluorescent Antibody TechniqueBiologyHIV AntibodiesMicrobiologyGiant CellsVirusMonocytesCell Linechemistry.chemical_compoundVirologymedicineHumansCells CulturedMonocyteFlow CytometryPhenotypeVirologymedicine.anatomical_structurechemistryGiant cellCell cultureCD4 AntigensHIV-1Viral diseaseGranulocytesMicrobiology and immunology
researchProduct

Increased immunosuppressive function of CD4(+)CD25(+)Foxp3(+)GITR+ T regulatory cells from NFATc2((-/-)) mice controls allergen-induced experimental …

2012

The expansion of effector T cells is tightly controlled by transcription factors like nuclear factor of activated T cells (NFAT) family members that mediate early intracellular responses to T cell receptor-mediated signals. In this study we show that, after allergen challenge, NFATc2((-/-)) mice had augmented number of functionally intact CD4(+)CD25(++)GITR(++) T regulatory (T regs) cells in the lung. Anti-GITR antibody treatment inhibited T regulatory cell function and enhanced the number of activated lung CD4(+) T cells associated with increased IL-2 and pSTAT-5 in the airways of NFATc2((-/-)) mice in experimental allergic asthma. This agonistic treatment led to increased inflammation in …

NFATC2T cellImmunologyInflammationBiologyT-Lymphocytes RegulatoryInterleukin 21MiceTh2 CellsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyAnimalsIL-2 receptorLungImmunosuppression TherapyMice KnockoutNFATC Transcription FactorsInterleukin-2 Receptor alpha SubunitFOXP3NFATForkhead Transcription FactorsHematologyAllergensAsthmarespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureImmunologyCD4 Antigensbiology.proteinCytokinesTh17 CellsFemalemedicine.symptomAntibodySpleenImmunobiology
researchProduct

Regulatory T cells selectively preserve immune privilege of self-antigens during viral central nervous system infection.

2012

Abstract Regulatory T cells (Tregs) are important for the attenuation of immune reactions. During viral CNS infections, however, an indiscriminate maintenance of CNS immune privilege through Treg-mediated negative regulation could prevent autoimmune sequelae but impair the control of viral replication. We analyzed in this study the impact of Tregs on the development of acute viral encephalomyelitis, T cell-mediated antiviral protection, and prevention of CNS autoimmunity following intranasal infection with the gliatropic mouse hepatitis virus strain A59. To assess the contribution of Tregs in vivo, we specifically depleted CD4+Foxp3+ T cells in a diphtheria toxin-dependent manner. We found …

Receptors CXCR3T cellImmunologychemical and pharmacologic phenomenaAutoimmunityBiologyCD8-Positive T-Lymphocytesmedicine.disease_causeCXCR3Lymphocyte ActivationAutoantigensT-Lymphocytes RegulatoryLymphocyte DepletionAutoimmunity03 medical and health sciencesMice0302 clinical medicineCentral Nervous System InfectionsImmune privilegeImmunitymedicineImmunology and AllergyAnimalsHumansEncephalomyelitisAdministration Intranasal030304 developmental biologyCell Proliferation0303 health sciencesImmunity CellularMice Inbred BALB CMurine hepatitis virusFOXP3hemic and immune systemsForkhead Transcription Factors3. Good healthmedicine.anatomical_structureViral replicationImmunologyAcute DiseaseCD4 AntigensLymph NodesCoronavirus InfectionsCD8030215 immunologyJournal of immunology (Baltimore, Md. : 1950)
researchProduct