Search results for "CD4+"

showing 10 items of 566 documents

CD4 blockade directly inhibits mouse and human CD4+ T cell functions independent of Foxp3+ Tregs

2013

CD4(+) helper T cells orchestrate protective immunity against pathogens, yet can also induce undesired pathologies including allergies, transplant rejection and autoimmunity. Non-depleting CD4-specific antibodies such as clone YTS177.9 were found to promote long-lasting T cell tolerance in animal models. Thus, CD4 blockade could represent a promising therapeutic approach for human autoimmune diseases. However, the mechanisms underlying anti-CD4-induced tolerance are incompletely resolved. Particularly, multiple immune cells express CD4 including Foxp3(+) regulatory T cells (Tregs) and dendritic cells (DCs), both controlling the activation of CD4(+)Foxp3(-) helper T cells. Utilizing mixed le…

T cellImmunologyPriming (immunology)Ki-1 Antigenchemical and pharmacologic phenomenaBiologyCD8-Positive T-LymphocytesLymphocyte ActivationT-Lymphocytes RegulatoryLymphocyte DepletionInterleukin 21MiceImmune systemmedicineImmune ToleranceImmunology and AllergyCytotoxic T cellAnimalsHumansIL-2 receptorCells CulturedAntilymphocyte SerumCell ProliferationMice Inbred BALB CFOXP3Forkhead Transcription Factorshemic and immune systemsDendritic CellsReceptors OX40medicine.diseaseTransplant rejectionMice Inbred C57BLmedicine.anatomical_structureImmunologyCD4 AntigensInterleukin-2
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Synergistic activation of dendritic cells by combined Toll-like receptor ligation induces superior CTL responses in vivo.

2006

Toll-like receptors (TLRs) are able to interact with pathogen-derived products and their signals induce the coordinated activation of innate and adaptive immune mechanisms. Dendritic cells (DCs) play a central role in these events. As the different TLRs are able to trigger MyD88/TRIF-dependent and -independent signaling pathways, we wondered if the simultaneous activation of these signaling cascades would synergize with respect to DC activation and induce superior cytotoxic T-lymphocyte (CTL) activity in vivo. We observed that indeed the combined activation of MyD88-dependent and -independent signaling induced by TLR7 and TLR3 ligands provoked a more rapid and more sustained bone marrow–der…

T-LymphocytesImmunologyBone Marrow CellsBiologyLigandsBiochemistryT-Lymphocytes RegulatoryMiceCytotoxic T cellAnimalsAntigen-presenting cellAdaptor Proteins Signal TransducingCD86Toll-like receptorCD40Membrane GlycoproteinsToll-Like ReceptorsImmunityhemic and immune systemsCell BiologyHematologyDendritic cellDendritic CellsAcquired immune systemCell biologyToll-Like Receptor 3Mice Inbred C57BLCTL*Toll-Like Receptor 7ImmunologyMyeloid Differentiation Factor 88biology.proteinSignal TransductionT-Lymphocytes CytotoxicBlood
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NFATc1 affects mouse splenic B cell function by controlling the calcineurin–NFAT signaling network

2011

Mouse B cells lacking NFATc1 exhibit defective proliferation, survival, isotype class switching, cytokine production, and T cell help.

T-LymphocytesImmunologyNaive B cellB-cell receptorReceptors Antigen B-CellLymphocyte ActivationArticleMice03 medical and health sciences0302 clinical medicinemedicineAnimalsImmunology and AllergyB cell030304 developmental biologyB-Lymphocytes0303 health sciencesCD40NFATC Transcription Factorsintegumentary systembiologyCalcineurinCD22Germinal centerImmunoglobulin Class SwitchingMolecular biology3. Good healthB-1 cellCalcineurinmedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchbiology.proteinCalciumSpleenSignal TransductionJournal of Experimental Medicine
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Tolerance without clonal expansion: self-antigen-expressing B cells program self-reactive T cells for future deletion.

2008

Abstract B cells have been shown in various animal models to induce immunological tolerance leading to reduced immune responses and protection from autoimmunity. We show that interaction of B cells with naive T cells results in T cell triggering accompanied by the expression of negative costimulatory molecules such as PD-1, CTLA-4, B and T lymphocyte attenuator, and CD5. Following interaction with B cells, T cells were not induced to proliferate, in a process that was dependent on their expression of PD-1 and CTLA-4, but not CD5. In contrast, the T cells became sensitive to Ag-induced cell death. Our results demonstrate that B cells participate in the homeostasis of the immune system by abl…

T-LymphocytesProgrammed Cell Death 1 ReceptorAutoimmunityAntigens CD/biosynthesisAntigens CD5/geneticsAutoantigensInterleukin 21MiceImmunology and AllergyCytotoxic T cellHomeostasisCTLA-4 AntigenIL-2 receptorAntigens Differentiation/biosynthesisB-LymphocytesAntigens CD/geneticsB-Lymphocytes/immunologyT-Lymphocytes/metabolismNatural killer T cellCell biologymedicine.anatomical_structureHomeostasis/immunology2723 Immunology and AllergyAntigens CD5/biosynthesisAntigens Differentiation/geneticsAntigens CD5/immunologyT cellImmunologyAntigens CD/immunologyClonal Deletion610 Medicine & healthchemical and pharmacologic phenomenaMice TransgenicBiologyAutoantigens/biosynthesisCD5 AntigensAutoimmunity/physiologyAutoantigens/immunologyAntigens CDmedicineAnimalsB-Lymphocytes/metabolismAntigen-presenting cellCell Proliferation2403 ImmunologyAntigens Differentiation/immunologyGene Expression Regulation/immunologyCD40Clonal Deletion/physiologyT-Lymphocytes/immunologyAntigens Differentiation10040 Clinic for NeurologyB-1 cellGene Expression Regulationbiology.protein
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Inefficient Termination of Antigen Responses in NF-ATp-Deficient Mice

1998

In order to elucidate the role of NF-ATp, one of the most prominent members of family of NF-AT transcription factors in peripheral T lymphocytes, in T cell activation and differentiation we created NF-ATp-deficient mice by gene targeting. Such NF-ATp-/- mice are born and appear to develop a normal immune system. Apart from clear-cut defects in the synthesis of mRNAs for Th2-type lymphokines, such as IL-4, IL-5, IL-10 and IL-13, in primary and secondary stimulations of spleen cells in vitro, of a distinct impaired deletion of V beta 11+/CD4+ T lymphocytes from these mice was detected after superantigen injection. Moreover, NF-ATp-/- mice older than 6 weeks show an 2-5 fold increase in number…

T-LymphocytesT cellImmunologyApoptosisCell CountEnterotoxinsMiceImmune systemAntigenSuperantigenmedicineAnimalsHumansImmunology and AllergyCell Line TransformedB-LymphocytesLymphokinesSuperantigensNFATC Transcription FactorsbiologyCD44LymphokineNuclear ProteinsGene targetingHematologyMolecular biologyDNA-Binding Proteinsmedicine.anatomical_structureCell culturebiology.proteinGene DeletionTranscription FactorsImmunobiology
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Development of spontaneous airway changes consistent with human asthma in mice lacking T-bet.

2002

Human asthma is associated with airway infiltration by T helper 2 (TH2) lymphocytes. We observed reduced expression of the TH1 transcription factor, T-bet, in T cells from airways of patients with asthma compared with that in T cells from airways of nonasthmatic patients, suggesting that loss of T-bet might be associated with asthma. Mice with a targeted deletion of the T-bet gene and severe combined immunodeficient mice receiving CD4+cells from T-bet knockout mice spontaneously demonstrated multiple physiological and inflammatory features characteristic of asthma. Thus, T-bet deficiency, in the absence of allergen exposure, induces a murine phenotype reminiscent of both acute and chronic h…

TBX21CD4-Positive T-LymphocytesAdoptive cell transferRatónchemical and pharmacologic phenomenaMice SCIDMicemedicineAnimalsHumansLungAsthmaMice KnockoutMultidisciplinarybusiness.industryRespiratory diseaseGene targetinghemic and immune systemsT lymphocyteAllergensmedicine.diseaseAdoptive TransferAsthmarespiratory tract diseasesDisease Models AnimalCollagen Type IIIKnockout mouseImmunologyGene TargetingCytokinesInterleukin-4Bronchial HyperreactivityInterleukin-5businessT-Box Domain ProteinsBronchoalveolar Lavage FluidTranscription FactorsScience (New York, N.Y.)
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Infectious Tolerance

2002

Regulatory CD4(+)CD25(+) T cells (Treg) are mandatory for maintaining immunologic self-tolerance. We demonstrate that the cell-cell contact-mediated suppression of conventional CD4(+) T cells by human CD25(+) Treg cells is fixation resistant, independent from membrane-bound TGF-beta but requires activation and protein synthesis of CD25(+) Treg cells. Coactivation of CD25(+) Treg cells with Treg cell-depleted CD4(+) T cells results in anergized CD4(+) T cells that in turn inhibit the activation of conventional, freshly isolated CD4(+) T helper (Th) cells. This infectious suppressive activity, transferred from CD25(+) Treg cells via cell contact, is cell contact-independent and partially medi…

TGF-βCD4-Positive T-Lymphocyteshuman regulatory T cellsT-LymphocytesImmunologyCellchemical and pharmacologic phenomenaIn Vitro TechniquesLymphocyte ActivationT-Lymphocytes RegulatoryImmune toleranceInterleukin 21AntigenTransforming Growth Factor betaCD4+CD25+ T cellsCell AdhesionImmune TolerancemedicineHumansImmunology and AllergyCytotoxic T cellIL-2 receptorbiologyBrief Definitive ReportModels ImmunologicalReceptors Interleukin-2hemic and immune systemsT-Lymphocytes Helper-InducerTransforming growth factor betainfectious tolerancemedicine.anatomical_structureT cell inhibitionImmunologyCancer researchbiology.proteinTransforming growth factorJournal of Experimental Medicine
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cIAP1-dependent TRAF2 degradation regulates the differentiation of monocytes into macrophages and their response to CD40 ligand.

2008

AbstractPeripheral blood monocytes are plastic cells that migrate to tissues and differentiate into various cell types, including macrophages, dendritic cells, and osteoclasts. We have described the migration of cellular inhibitor of apoptosis protein 1 (cIAP1), a member of the IAP family of proteins, from the nucleus to the Golgi apparatus in monocytes undergoing differentiation into macrophages. Here we show that, once in the cytoplasm, cIAP1 is involved in the degradation of the adaptor protein tumor necrosis factor receptor–associated factor 2 (TRAF2) by the proteosomal machinery. Inhibition of cIAP1 prevents the decrease in TRAF2 expression that characterizes macrophage formation. We d…

TRAF2CytoplasmCellular differentiationImmunologyCD40 LigandDown-RegulationGene ExpressionGolgi ApparatusBiologyBiochemistryMonocytesProinflammatory cytokineInhibitor of Apoptosis ProteinsPhagocytes Granulocytes and MyelopoiesisPhagocytosisMacrophageHumansRNA Small InterferingCD40U937 cellMacrophagesSignal transducing adaptor proteinCell DifferentiationCell BiologyHematologyU937 CellsTNF Receptor-Associated Factor 2Molecular biologyCell biologybiology.proteinTumor necrosis factor alphaBlood
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Measurements of Collisional Line Widths in the Stimulated Raman Q-Branch of the v1 Band of Silane

1990

0377-0486; Self-broadened widths of 28SiH4 in the v1 Q-branch have been measured at room temperature (295 K) using high-resolution stimulated Raman spectroscopy. These collisional widths have been obtained by fitting a superposition of Voigt profiles to the experimental spectra in the pressure range 28-154 Torr. No evidence for line mixing within the tetrahedral components of a Q(J) line has been found. The line broadening coefficients for J up to 13 depend weakly on the rotational quantum number. The mean value is 103.7 x 10(-3) cm-1 atm-1.

TUNABLE DIODE-LASERINFRARED DOUBLE-RESONANCEENERGY-TRANSFERMETHANE 13CD4REGION
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Identificazione di nuovi bersagli terapeutici nel microambiente nei Linfomi T Epatosplenici

Target terapeuticiAnticorpi MonoclonaliLinfoma T EpatosplenicoPSGL-1CD44Linfoma T Epatosplenico; Target terapeutici; Anticorpi Monoclonali; PSGL-1; CD44
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