Search results for "CD"

showing 10 items of 4072 documents

Trial Watch: Adoptively transferred cells for anticancer immunotherapy

2017

IF 7.719; International audience; Immunotherapies aimed at strengthening immune effector responses against malignant cells are growing at exponential rates. Alongside, the impressive benefits obtained by patients with advanced melanoma who received adoptively transferred tumor-infiltrating lymphocytes (TILs) have encouraged the scientific community to pursue adoptive cell transfer (ACT)-based immunotherapy. ACT involves autologous or allogenic effector lymphocytes that are generally obtained from the peripheral blood or resected tumors, expanded and activated ex vivo, and administered to lymphodepleted patients. ACT may be optionally associated with chemo- and/or immunotherapeutics, with th…

lcsh:Immunologic diseases. Allergy0301 basic medicinePD-L1Adoptive cell transferBreakthrough therapymedicine.medical_treatmentImmunology[SDV.CAN]Life Sciences [q-bio]/CancerReviewBiologycytotoxic T lymphocytelcsh:RC254-282CD19[ SDV.CAN ] Life Sciences [q-bio]/Cancer03 medical and health sciences0302 clinical medicineAntigenPD-L1PD-1medicineImmunology and AllergyCytotoxic T cellNK cellchimeric antigen receptorImmunotherapylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensChimeric antigen receptor3. Good healthimmune checkpoint blockers030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologybiology.proteinlcsh:RC581-607
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Azithromycin Differentially Alters TCR-Activated Helper T Cell Subset Phenotype and Effector Function

2020

In addition to their antibiotic activities, azithromycin (AZM) exhibits anti-inflammatory effects in various respiratory diseases. One of the potent anti-inflammatory mechanisms is through inhibition of CD4+ helper T (Th) cell effector function. However, their impact on specific Th subset is obscure. Herein, we demonstrate the cellular basis of phenotypic and functional alterations associated with Th subsets following AZM treatment in vitro. Using well-characterized Th subset specific chemokine receptors, we report significant suppression of T cell receptor (TCR)-stimulated hyperactivated CCR4+CXCR3+ (Th0) expansion compared to CCR4-CXCR3+ (Th1-like) and CCR4+CXCR3- (Th2-like) cells. Intere…

lcsh:Immunologic diseases. Allergy0301 basic medicineReceptors CCR4Receptors CXCR3Receptor expressionImmunologyReceptors Antigen T-CellBiologyCXCR303 medical and health sciencesChemokine receptorInterferon-gamma0302 clinical medicineDownregulation and upregulationCell MovementT-Lymphocyte SubsetsImmunology and AllergyHumansIFN-γInterleukin 4Cells CulturedOriginal Researchanti-inflammatoryazithromycinCD4+ helper T cellsCXCR3EffectorCell growthT-cell receptorIL-4apoptosisCell DifferentiationBacterial InfectionsTh1 CellsHealthy VolunteersCell biologyAnti-Bacterial Agents030104 developmental biologyCCR4Interleukin-4lcsh:RC581-607030215 immunologyFrontiers in Immunology
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RUNX3 and T-Bet in Immunopathogenesis of Ankylosing Spondylitis—Novel Targets for Therapy?

2019

Susceptibility to ankylosing spondylitis (AS) is polygenic with more than 100 genes identified to date. These include HLA-B27 and the aminopeptidases (ERAP1, ERAP2, and LNPEPS), which are involved in antigen processing and presentation to T-cells, and several genes (IL23R, IL6R, STAT3, JAK2, IL1R1/2, IL12B, and IL7R) involved in IL23 driven pathways of inflammation. AS is also strongly associated with polymorphisms in two transcription factors, RUNX3 and T-bet (encoded by TBX21), which are important in T-cell development and function. The influence of these genes on the pathogenesis of AS and their potential for identifying drug targets is discussed here.

lcsh:Immunologic diseases. Allergy0301 basic medicineTBX21Mini ReviewImmunologyBiologyCD8-Positive T-Lymphocytesmedicine.disease_causeAminopeptidasesInterleukin-23Polymorphism Single NucleotideAutoimmunity03 medical and health sciences0302 clinical medicineankylosing spondylitisInterleukin 23medicineImmunology and AllergyHumansImmunologic FactorsSpondylitis AnkylosingMolecular Targeted TherapyInterleukin-7 receptorTranscription factorHLA-B27 AntigenAnkylosing spondylitistherapyAntigen processingautoimmunityReceptors Interleukinmedicine.disease3. Good healthKiller Cells Natural030104 developmental biologyCore Binding Factor Alpha 3 SubunitGene Expression RegulationinflammationImmunologylcsh:RC581-607T-Box Domain ProteinsFunctional genomicsfunctional genomics030215 immunologyFrontiers in Immunology
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Evolution of melanoma cross-resistance to CD8⁺ T cells and MAPK inhibition in the course of BRAFi treatment

2018

The profound but frequently transient clinical responses to BRAFV600 inhibitor (BRAFi) treatment in melanoma emphasize the need for combinatorial therapies. Multiple clinical trials combining BRAFi and immunotherapy are under way to further enhance therapeutic responses. However, to which extent BRAFV600 inhibition may affect melanoma immunogenicity over time remains largely unknown. To support the development of an optimal treatment protocol, we studied the impact of prolonged BRAFi exposure on the recognition of melanoma cells by T cells in different patient models. We demonstrate that autologous CD8+ tumor-infiltrating lymphocytes (TILs) efficiently recognized short-term (3, 7 days) BRAF…

lcsh:Immunologic diseases. Allergy0301 basic medicinecd8+ t cellsmedicine.medical_treatmentT cellImmunologyMedizinlcsh:RC254-282mekresistance03 medical and health sciences0302 clinical medicineAntigenantigensmelanomaImmunology and AllergyMedicineCytotoxic T cellbusiness.industryMelanomaImmunotherapylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseTumor antigeninhibitor030104 developmental biologymedicine.anatomical_structureOncologyCSPG4030220 oncology & carcinogenesisCancer researchlcsh:RC581-607businessbrafCD8
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A multicenter phase 1 study of solitomab (MT110, AMG 110), a bispecific EpCAM/CD3 T-cell engager (BiTE®) antibody construct, in patients with refract…

2018

ABSTRACT We assessed the tolerability and antitumor activity of solitomab, a bispecific T-cell engager (BiTE®) antibody construct targeting epithelial cell adhesion molecule (EpCAM). Patients with relapsed/refractory solid tumors not amenable to standard therapy received solitomab as continuous IV infusion in a phase 1 dose-escalation study with six different dosing schedules. The primary endpoint was frequency and severity of adverse events (AEs). Secondary endpoints included pharmacokinetics, pharmacodynamics, immunogenicity, and antitumor activity. Sixty-five patients received solitomab at doses between 1 and 96 µg/day for ≥28 days. Fifteen patients had dose-limiting toxicities (DLTs): e…

lcsh:Immunologic diseases. Allergy0301 basic medicinemedicine.medical_specialtyImmunologyAMG 110bispecificlcsh:RC254-282Gastroenterology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSolitomabRefractoryPharmacokineticsInternal medicineImmunology and AllergyMedicineAdverse effectOriginal Researchbusiness.industryEpCAM phase 1Epithelial cell adhesion moleculesolitomablcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensBiTE®CD3Discontinuation030104 developmental biologyMT110OncologyTolerabilitychemistry030220 oncology & carcinogenesisPharmacodynamicssolid tumorimmunotherapylcsh:RC581-607businessOncoimmunology
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Responsiveness to anti-PD-1 and anti-CTLA-4 immune checkpoint blockade in SB28 and GL261 mouse glioma models.

2018

Immune checkpoint blockade (ICB) is currently evaluated in patients with glioblastoma (GBM), based on encouraging clinical data in other cancers, and results from studies with the methylcholanthrene-induced GL261 mouse glioma. In this paper, we describe a novel model faithfully recapitulating some key human GBM characteristics, including low mutational load, a factor reported as a prognostic indicator of ICB response. Consistent with this observation, SB28 is completely resistant to ICB, contrasting with treatment sensitivity of the more highly mutated GL261. Moreover, SB28 shows features of a poorly immunogenic tumor, with low MHC-I expression and modest CD8(+) T-cell infiltration, suggest…

lcsh:Immunologic diseases. Allergy0301 basic medicinemedicine.medical_treatmentGL261ImmunologyOncology and CarcinogenesisMajor histocompatibility complexMalignancylcsh:RC254-282Mutational loadVaccine Related03 medical and health sciences0302 clinical medicineRare DiseasesGliomamedicineImmunology and Allergyddc:576.5sb28mutational loadCancerddc:616biologybusiness.industryBrief ReportSB28glioblastomaNeurosciencesImmunotherapyimmune checkpoint blockadelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseImmune checkpointBlockadeBrain DisordersBrain Cancer030104 developmental biologyOncologygl261030220 oncology & carcinogenesisCancer researchbiology.proteinImmunizationlcsh:RC581-607businessGlioblastomaCD8Immune checkpoint blockadeGlioblastoma
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Human γδ T-Cells: From Surface Receptors to the Therapy of High-Risk Leukemias

2018

γδ T lymphocytes are potent effector cells, capable of efficiently killing tumor and leukemia cells. Their activation is mediated by γδ T-cell receptor (TCR) and by activating receptors shared with NK cells (e.g., NKG2D and DNAM-1). γδ T-cell triggering occurs upon interaction with specific ligands, including phosphoantigens (for Vγ9Vδ2 TCR), MICA-B and UL16 binding protein (for NKG2D), and PVR and Nectin-2 (for DNAM-1). They also respond to cytokines undergoing proliferation and release of cytokines/chemokines. Although at the genomic level γδ T-cells have the potential of an extraordinary TCR diversification, in tissues they display a restricted repertoire. Recent studies have identified …

lcsh:Immunologic diseases. Allergy0301 basic medicineαβ T-cellChemokineB-cell depletion; hematopoietic stem cells; HLA-haploidentical transplantation; receptors; αβ T-cell; γδ T-cellsReceptors Antigen T-Cell alpha-betaMini ReviewHLA-haploidentical transplantationImmunologyGenes MHC Class Ichemical and pharmacologic phenomenaMajor histocompatibility complexCD19Mice03 medical and health sciencesγδ T-cellsAntigenReceptorsMHC class ImedicineAnimalsHumansImmunology and AllergyIntraepithelial LymphocytesB-LymphocytesLeukemiaB-cell depletionbiologyT-cell receptorHematopoietic Stem Cell Transplantationmedicine.diseaseNKG2DKiller Cells NaturalLeukemia030104 developmental biologySettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICACytomegalovirus InfectionsImmunologybiology.proteinlcsh:RC581-607Hematopoietic stem cellsFrontiers in Immunology
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Age and immunity

2006

Abstract Longitudinal studies are defining progressive alterations to the immune system associated with increased mortality in the very elderly. Many of these changes are exacerbated by or even caused by chronic T cell stimulation by persistent antigen, particularly from Cytomegalovirus. The composition of T cell subsets, their functional integrity and representation in the repertoire are all markedly influenced by age and by CMV. How these findings relate to epidemiological, functional, genetic, genomic and proteomic studies of human T cell immunosenescence was the subject of intense debate at an international conference held just before Christmas 2005 in the Black Forest.

lcsh:Immunologic diseases. AllergyAgingbiologyT cellRepertoireImmunologyShort ReportCongenital cytomegalovirus infectionImmunosenescencelcsh:Geriatricsmedicine.diseaseaged aging apoptosis article CD4+ CD25+ T lymphocytelcsh:RC952-954.6Immune systemmedicine.anatomical_structureAntigenImmunityImmunologybiology.proteinmedicineAntibodylcsh:RC581-607
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Role of persistent CMV infection in configuring T cell immunity in the elderly

2007

Abstract Ageing is associated with declines in many physiological parameters, including multiple immune system functions. The rate of acceleration of the frequency of death due to cardiovascular disease or cancer seems to increase with age from middle age up to around 80 years, plateauing thereafter. Mortality due to infectious disease, however, does not plateau, but continues to accelerate indefinitely. The elderly commonly possess oligoclonal expansions of T cells, especially of CD8 cells, which, surprisingly, are often associated with cytomegalovirus (CMV) seropositivity. This in turn is associated with many of the same phenotypic and functional alterations to T cell immunity that have b…

lcsh:Immunologic diseases. AllergyAgingbiologybusiness.industryImmunologyMembrane raftReviewDiseaseImmunosenescencelcsh:GeriatricsBioinformaticsVaccinationlcsh:RC952-954.6aged aging antigen expression apoptosis cancer incidence CD4+ T lymphocyte CD8+ T lymphocyte cellular immunityAgeingImmune systemInfectious disease (medical specialty)ImmunityImmunologybiology.proteinMedicineAntibodybusinesslcsh:RC581-607Immunity & Ageing
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Protection of Mice from Acute Graft-versus-Host Disease Requires CD28 Co-stimulation on Donor CD4+ Foxp3+ Regulatory T Cells

2017

Acute graft-versus-host disease (aGvHD) is a major cause of morbidity and mortality after allogeneic hematopoietic stem cell plus T cell transplantation (allo-HSCT). In this study, we investigated the requirement for CD28 co-stimulation of donor CD4\(^{+}\) conventional (CD4\(^{+}\)CD25\(^{-}\)Foxp3\(^{-}\), Tconv) and regulatory (CD4\(^{+}\)CD25\(^{+}\)Foxp3\(^{+}\), Treg) T cells in aGvHD using tamoxifen-inducible CD28 knockout (iCD28KO) or wild-type (wt) littermates as donors of CD4\(^{+}\) Tconv and Treg. In the highly inflammatory C57BL/6 into BALB/c allo-HSCT transplantation model, CD28 depletion on donor CD4\(^{+}\) Tconv reduced clinical signs of aGvHD, but did not significantly pro…

lcsh:Immunologic diseases. AllergyCD28acute graft-versus-host diseaseImmunologyco-stimulationhemic and immune systemschemical and pharmacologic phenomenainducible deletionregulatory T cellssurgical procedures operativeimmune system diseaseshemic and lymphatic diseasesImmunology and Allergyddc:610lcsh:RC581-607Frontiers in Immunology
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