Search results for "T cell"

showing 10 items of 2228 documents

miR-155expression in antitumor immunity: The higher the better?

2019

MicroRNAs are small noncoding RNAs that modulate gene expression either directly, by impairing the stability and/or translation of transcripts that contain their specific target sequence, or indirectly through the targeting of transcripts that encode transcription factors, factors implicated in signal transduction pathways, or epigenetic regulators. Abnormal expression of micro-RNAs has been found in nearly all types of pathologies, including cancers. MiR-155 has been the first microRNA to be implicated in the regulation of the innate and adaptative immune responses, and its expression is either increased or decreased in a variety of liquid and solid malignancies. In this review, we examine…

Cancer ResearchLeukemiaCarcinogenesisBiologymiR-155MicroRNAs03 medical and health sciences0302 clinical medicineImmune system030220 oncology & carcinogenesisGene expressionmicroRNAGeneticsCancer researchAnimalsHumansCytotoxic T cellTumor EscapeImmunotherapyEpigeneticsDown SyndromeSignal transductionTranscription factorGenes, Chromosomes and Cancer
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Cytolytic T cell reactivity against melanoma-associated differentiation antigens in peripheral blood of melanoma patients and healthy individuals

1996

Antigenic peptides derived from several differentiation antigens of the melanocyte lineage were recently identified in human melanomas as targets for HLA-A2.1-restricted cytotoxic T lymphocytes (CTLs). To examine their potential role in tumour-directed immune responses in vivo, we determined CTL reactivity against seven antigenic peptides derived from the Melan A/MART-1, tyrosinase and gp100/Pmel17 antigens in the peripheral blood of 10 HLA-A2+ healthy controls and 26 HLA-A2+ melanoma patients. The influenza matrix peptide (GILGFVFTL) presented by HLA-A2.1 was used as a control peptide. CTL reactivity was assessed in a mixed lymphocyte 'peptide' culture assay. Reactivity against Melan A/MAR…

Cancer ResearchLymphocyte10050 Institute of Pharmacology and Toxicology610 Medicine & healthDermatologyPeripheral blood mononuclear cell2708 DermatologyMART-1 AntigenImmune systemMelanocyte differentiationAntigenAntigens NeoplasmTumor Cells CulturedmedicineHumansCytotoxic T cell1306 Cancer ResearchAmino Acid SequenceMelanomaneoplasmsMembrane GlycoproteinsMonophenol Monooxygenasebusiness.industryMelanomaProteinsmedicine.diseaseAntigens DifferentiationNeoplasm ProteinsCTL*medicine.anatomical_structureOncologyImmunology570 Life sciences; biology2730 OncologybusinessT-Lymphocytes Cytotoxicgp100 Melanoma AntigenMelanoma Research
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Cellular immune response to human renal-cell carcinomas: Definition of a common antigen recognized by HLA-A2-restricted cytotoxic T-Lymphocyte (CTL) …

1994

Cytotoxic T lymphocyte (CTL) clones directed against autologous renal-cell carcinoma (RCC) cell lines were generated by mixed lymphocyte/tumor-cell culture (MLTC) using peripheral blood lymphocytes (PBL). A CD8+, CD4- CTL clone MZ1257-CTL 5/30 with high cytolytic activity for the autologous tumor cell line MZ1257-RCC was established. No lysis of the autologous EBV-transformed B lymphocytes (EBV-B) or K562 cells was observed. A panel of HLA-A2-matched allogeneic RCC lines was recognized by CTL 5/30. Further specificity analysis showed a cross-reactivity with HLA-A2-matched allogeneic tumor cells of various origins, especially melanoma. CTL 5/30 was also cross-reactive with several HLA-A2-pos…

Cancer ResearchLymphocyteCross ReactionsBiologyKidneyImmune systemAntigenAntigens NeoplasmHLA-A2 AntigenTumor Cells CulturedmedicineHumansCytotoxic T cellCarcinoma Renal CellMelanomaImmunity CellularHistocompatibility Antigens Class IAntibodies MonoclonalT lymphocyteAntigens DifferentiationAutologous tumor cellKidney NeoplasmsCTL*medicine.anatomical_structureOncologyImmunologyLymphocyte Culture Test MixedClone (B-cell biology)T-Lymphocytes CytotoxicInternational Journal of Cancer
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In vivo targeting of human neutralizing antibodies against CD55 and CD59 to lymphoma cells increases the antitumor activity of rituximab.

2007

AbstractAn in vivo model of human CD20+ B-lymphoma was established in severe combined immunodeficiency mice to test the ability of human neutralizing miniantibodies to CD55 and CD59 (MB55 and MB59) to enhance the therapeutic effect of rituximab. The miniantibodies contained single-chain fragment variables and the hinge-CH2-CH3 domains of human IgG1. LCL2 cells were selected for the in vivo study among six B-lymphoma cell lines for their high susceptibility to rituximab-dependent complement-mediated killing enhanced by MB55 and MB59. The cells injected i.p. primarily colonized the liver and spleen, leading to the death of the animals within 30 to 40 days. Thirty percent of mice receiving bio…

Cancer ResearchLymphoma B-Cellmedicine.drug_classmedicine.medical_treatmentAntineoplastic AgentsCD59 AntigensAntigens CD59Mice SCIDPharmacologyMonoclonal antibodyAntigens CD55Antineoplastic AgentAntibodies Monoclonal Murine-DerivedMicerituximabIn vivomedicineAnimalsHumansantibodies against CD55 and CD59CD20Severe combined immunodeficiencyMice Inbred BALB CbiologyCD55 AntigensAnimalAntibody-Dependent Cell CytotoxicityAntibodies MonoclonalImmunotherapyrituximab; antibodies against CD55 and CD59medicine.diseaseDisease Models AnimalOncologyAnimals; Antibodies Monoclonal; Antibodies Monoclonal Murine-Derived; Antibody-Dependent Cell Cytotoxicity; Antigens CD55; Antigens CD59; Antineoplastic Agents; Disease Models Animal; Female; Humans; Lymphoma B-Cell; Mice; Mice Inbred BALB C; Mice SCID; Rituximab; Cancer Research; OncologyMonoclonalImmunologybiology.proteinRituximabFemaleAntibodymedicine.drugHuman
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Bispecific antibodies targeting tumor-associated antigens and neutralizing complement regulators increase the efficacy of antibody-based immunotherap…

2015

The efficacy of antibody-based immunotherapy is due to the activation of apoptosis, the engagement of antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity (CDC). We developed a novel strategy to enhance CDC using bispecific antibodies (bsAbs) that neutralize the C-regulators CD55 and CD59 to enhance C-mediated functions. Two bsAbs (MB20/55 and MB20/59) were designed to recognize CD20 on one side. The other side neutralizes CD55 or CD59. Analysis of CDC revealed that bsAbs could kill 4-25 times more cells than anti-CD20 recombinant antibody in cell lines or cells isolated from patients with chronic lymphocytic leukemia. The pharmacokinetics of the bsAbs was evaluate…

Cancer ResearchLymphomaMacrophageChronic lymphocytic leukemiamedicine.medical_treatmentAntibodieCell SeparationMice SCIDMiceAntibodies BispecificCloning MolecularCytotoxicityCD20LeukemiabiologyCD55 AntigensMedicine (all)HematologyFlow CytometryBurkitt LymphomaKiller Cells NaturalLeukemiaOncologyFemaleImmunotherapyAntibodybispecific antibodiesExperimental Lymphoma Mice MiceHumanComplement System ProteinCD59 AntigensEnzyme-Linked Immunosorbent AssayAntigens CD59Antigens CD55AntibodiesExperimentalAntigenbispecific antibodies; Leukemia; Experimental Lymphoma Mice Mice; complement systemmedicineAnimalsHumanscomplement systemAnimalMacrophagesAntibody-Dependent Cell CytotoxicityImmunotherapyComplement System Proteinsmedicine.diseaseAntigens CD20Complement systembispecific antibodieDisease Models AnimalAnesthesiology and Pain MedicineMicroscopy FluorescenceImmunologybiology.protein
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Abstract A110: Mutant MHC class II epitopes drive therapeutic immune responses to cancer

2016

Abstract Mutations are regarded as ideal targets for cancer immunotherapy. As neoepitopes with strict lack of expression in any healthy tissue, they are expected to be safe and could bypass the central tolerance mechanisms. Recent advances in nucleic acid sequencing technologies have revolutionized the field of genomics, allowing the readily targeting of mutated neoantigens for personalized cancer vaccination. We demonstrated in three independent murine tumor models that a considerable fraction of non-synonymous cancer mutations is immunogenic and that unexpectedly the immunogenic mutanome is pre-dominantly recognized by CD4+ T cells. RNA vaccination with such MHC class II restricted immuno…

Cancer ResearchMHC class IIbiologymedicine.medical_treatmentT cellImmunologyVirologyEpitopemedicine.anatomical_structureAntigenCancer immunotherapybiology.proteinmedicineCancer vaccineCentral toleranceCD8Cancer Immunology Research
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Molecular mechanisms of HLA class I antigen abnormalities following viral infection and transformation.

2005

In humans as in other animal species, CD8+ cytotoxic T lymphocytes (CTLs) play an important if not the major role in controlling virus-infected and malignant cell growth. The interactions between CD8+ T cells and target cells are mediated by human leukocyte antigen (HLA) class I antigens loaded with viral and tumor antigen-derived peptides along with costimulatory receptor/ligand stimuli. Thus, to escape from CD8+ T-cell recognition and destruction, viruses and tumor cells have developed strategies to inhibit the expression and/or function of HLA class I antigens. In contrast, cells with downregulated MHC class I surface expression can be recognized by NK cells, although NK cell-mediated ly…

Cancer ResearchMacromolecular SubstancesDown-RegulationGenes MHC Class IHuman leukocyte antigenCD8-Positive T-LymphocytesNatural killer cellAntigenHLA AntigensNeoplasmsMHC class IViral InterferencemedicineCytotoxic T cellHumansAntigen-presenting cellbiologyMHC class I antigenAntigen processingmedicine.anatomical_structureOncologyVirus DiseasesImmunologybiology.proteinImmunotherapySignal TransductionInternational journal of cancer
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Blood T-cell Vβ transcriptome in melanoma patients

2004

Tumor-cells have been shown to elicit MHC-restricted and antigen-specific T-cell responses. In this article, we used a new approach to study T-cell responses in tumor-bearing patients based on a global representation of the Vβ-transcriptome, making it possible to grade CDR3-length distribution (CDR3-LD) alterations. Six patients with advanced melanoma disease, from whom blood samples were taken before and serially after tyrosinase-A peptide vaccination, were studied. The PBMC from patients displayed highly significant Vβ transcriptome alterations as compared to healthy individuals. Similar Vβ alterations could be detected both in PBMCs and at the tumor site. After vaccination, Vβ alteration…

Cancer ResearchMelanomaT cellT-cell receptorT lymphocyteBiologymedicine.diseasePeripheral blood mononuclear cellTranscriptomeImmune systemmedicine.anatomical_structureOncologyHypoxanthine-guanine phosphoribosyltransferaseImmunologymedicineInternational Journal of Cancer
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Nanofitins targeting heat shock protein 110: an innovative immunotherapeutic modality in cancer.

2021

The presence of an inactivating heat shock protein 110 (HSP110) mutation in colorectal cancers has been correlated with an excellent prognosis and with the ability of HSP110 to favor the formation of tolerogenic (M2-like) macrophages. These clinical and experimental results suggest a potentially powerful new strategy against colorectal cancer: the inhibition of HSP110. In this work, as an alternative to neutralizing antibodies, Nanofitins (scaffold ~7 kDa proteins) targeting HSP110 were isolated from the screening of a synthetic Nanofitin library, and their capacity to bind (immunoprecipitation, biolayer interferometry) and to inhibit HSP110 was analyzed in vitro and in vivo. Three Nanofiti…

Cancer ResearchMice03 medical and health sciencesLymphocytes Tumor-Infiltrating0302 clinical medicineImmune systemPeptide LibraryIn vivoCell Line TumorHeat shock proteinTumor MicroenvironmentmedicineAnimalsHumansCytotoxic T cellHSP110 Heat-Shock Proteinssmall peptide moleculesTumor microenvironmentanticancer targeted therapybiologyChemistryMacrophagesCancer[SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciencesmedicine.diseaseXenograft Model Antitumor AssaysPeptide FragmentsIn vitro3. Good healthNanofitinsOncologyPositron-Emission Tomography030220 oncology & carcinogenesisbiology.proteinCancer researchFemaleAntibodyColorectal NeoplasmsHSP110
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Acute myeloid leukemia (AML)-reactive cytotoxic T lymphocyte clones rapidly expanded from CD8(+) CD62L((high)+) T cells of healthy donors prevent AML…

2008

Objective Current in vitro techniques for isolating leukemia-reactive cytotoxic T lymphocytes (CTLs) from healthy donors are of relatively low efficiency and yield responder populations with unknown biological significance. This study aimed at the development of a more reliable approach, allowing generation and expansion of acute myeloid leukemia (AML)-reactive CTLs using primary in vitro stimulation. Materials and Methods We established allogeneic mini-mixed lymphocyte-leukemia cultures (mini-MLLCs) by stimulating donor CD8 + T cells with human leukocyte antigen (HLA) class I–matched AML blasts in microtiter plates. Before culture, CD8 + T cells were separated into CD62L (high)+ and CD62L …

Cancer ResearchMyeloidGenes MHC Class Ichemical and pharmacologic phenomenaHuman leukocyte antigenMice SCIDBiologyCD8-Positive T-LymphocytesMiceImmune systemMice Inbred NODhemic and lymphatic diseasesGeneticsmedicineCytotoxic T cellAnimalsHumansL-SelectinMolecular BiologyAllelesCells CulturedMice KnockoutMyeloid leukemiahemic and immune systemsCell BiologyHematologyReference Standardsmedicine.diseaseCytotoxicity Tests ImmunologicClone CellsCTL*LeukemiaLeukemia Myeloid Acutemedicine.anatomical_structureImmunologyCD8Neoplasm TransplantationInterleukin Receptor Common gamma SubunitT-Lymphocytes CytotoxicExperimental hematology
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