Search results for "Compatibility"

showing 10 items of 859 documents

Stalemating a clever opportunist: lessons from murine cytomegalovirus.

2003

Abstract Cytomegaloviruses and their specific hosts have come to an arrangement that avoids disease but allows the viruses to persist in the individual host and to spread in the host species. Recent work has uncovered some of the molecular details of this evolutionary “contract for mutual survival.” Cytomegaloviruses encode proteins, referred to as “immunoevasins,” which are specifically committed to subvert the immune defense of the host for evading virus elimination. In reply, the hosts have evolved countermeasures to overcome the viral immunoevasins and present antigenic peptides to an extent that is sufficient for confining virus replication to below a harmful level. Accordingly, cytome…

ImmunologyAntigen presentationCongenital cytomegalovirus infectionDown-RegulationDiseaseImmunodominanceBiologyCD8-Positive T-LymphocytesMajor histocompatibility complexInterferon-gammaMiceViral ProteinsViral Envelope ProteinsmedicineImmunology and AllergyCytotoxic T cellAnimalsImmunologic SurveillanceGlycoproteinsAntigen PresentationMembrane GlycoproteinsCytomegalic inclusion diseaseHistocompatibility Antigens Class IModels ImmunologicalGeneral Medicinemedicine.diseaseVirologyPeptide FragmentsProtein TransportViral replicationCytomegalovirus Infectionsbiology.proteinCarrier ProteinsHuman immunology
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Macrophages Escape Inhibition of Major Histocompatibility Complex Class I-Dependent Antigen Presentation by Cytomegalovirus

2000

ABSTRACTThe mouse cytomegalovirus (MCMV)m152- andm06-encoded glycoproteins gp40 and gp48, respectively, independently downregulate major histocompatibility complex (MHC) class I surface expression during the course of productive MCMV infection in fibroblasts. As a result, presentation of an immediate-early protein pp89-derived nonapeptide toH-2Ld-restricted CD8+cytotoxic T cells is completely prevented in fibroblasts. Here we demonstrate that MCMV-infected primary bone marrow macrophages and the macrophage cell line J774 constitutively present pp89 peptides during permissive MCMV infection to cytotoxic T lymphocytes (CTL). In contrast to fibroblasts, expression of them152andm06genes in macr…

ImmunologyAntigen presentationCytomegalovirusBone Marrow CellsCD8-Positive T-LymphocytesMajor histocompatibility complexMicrobiologyCell LineImmediate-Early ProteinsMiceViral ProteinsViral Envelope ProteinsVirologyMHC class IAnimalsCytotoxic T cellAntigen-presenting cellAntigen PresentationMice Inbred BALB CMembrane GlycoproteinsbiologyAntigen processingMacrophagesHistocompatibility Antigens Class IMHC restrictionMolecular biologyInsect Sciencebiology.proteinPathogenesis and ImmunityCD8Journal of Virology
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C4 DNA RFLP reference typing report.

1990

One hundred and three individual DNA samples (including 23 families) were studied at the gene level during the reference typing of the fourth component of human complement at the VIth Complement Genetics Workshop in Mainz (1989). All samples were analyzed with the restriction enzyme Taq I and with two DNA probes recognizing the 5' ends of both C4 genes and the two adjacent 21-hydroxylase genes. This RFLP is informative for the number of C4 genes as well as for their respective gene size. We found a high degree of variation regarding the number of C4 genes, i.e. haplotypes with 1-3 structural C4 genes of 16 or 22 kb size. By correlating these haplotypes to the complotypes obtained by protein…

ImmunologyBiologyMajor Histocompatibility Complexchemistry.chemical_compoundHumansTypingDeoxyribonucleases Type II Site-SpecificGeneAllelesGeneticsModels GeneticHybridization probeHaplotypeGenetic VariationComplement C4HematologyDNARestriction enzymeBlotting SouthernchemistryHaplotypesMultilocus sequence typingSteroid 21-HydroxylaseRestriction fragment length polymorphismDNAPolymorphism Restriction Fragment LengthComplement and inflammation
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Synthesis and expression of MHC class II molecules in the absence of attached invariant chains by recombinant-interferon-gamma-activated bone-marrow-…

1987

Pure populations of in vitro propagated bone marrow-derived macrophages are constitutively Ia negative. Co-culturing of these cells with recombinant interferon-gamma (rIFN-gamma) resulted in the appearance of high amounts of Ia antigens at the cell surface of essentially all cells. The continuous presence of the stimulus was a prerequisite for sustained Ia expression because removal of the stimulus resulted in rapid decline of surface Ia. Two-dimensional (2D) gel analysis (1D isoelectric focusing, 2D sodium dodecyl sulfate-polyacrylamide gel electrophoresis) of class II molecules synthesized by rIFN-gamma-stimulated bone marrow macrophages (BMM phi) revealed that, in contrast to class II co…

ImmunologyBone Marrow Cellslaw.inventionInterferon-gammaMicelawImmunology and AllergyAnimalsNorthern blotRNA MessengerGel electrophoresisMessenger RNAMHC class IIMice Inbred C3HPolymorphism GeneticbiologyIsoelectric focusingMacrophagesHistocompatibility Antigens Class IIDNAMacrophage ActivationMolecular biologyIn vitroRecombinant ProteinsGene Expression RegulationRecombinant DNAbiology.proteinIntracellularEuropean journal of immunology
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Impact of MHC class I alleles on the M. tuberculosis antigen-specific CD8+ T-cell response in patients with pulmonary tuberculosis

2007

Challenged by scattered understanding of protective immunity to Mycobacterium tuberculosis (MTB), we have mapped peptide epitopes to human leukocyte antigen (HLA)-A*0101, A*0201, A*1101, A*2402, B*0702, B*0801 and B*1501 of the secreted mycobacterial antigen Ag85B, a vaccine candidate that may be associated with immune protection. Affinity (ED(50)) and half-life (t(1/2), off-rate) analysis for individual peptide species on HLA-A and HLA-B molecules revealed binding ranges between 10(-3) and 10(-7) M. After selection of the best matches, major histocompatibility complex class I/peptide tetramer complexes were constructed to measure the CD8+ T-cell responses directly ex vivo in peripheral blo…

ImmunologyGenes MHC Class IPeptide bindingHuman leukocyte antigenCD8-Positive T-LymphocytesMajor histocompatibility complexEpitopeMycobacterium tuberculosisMHC class IGeneticsHumansCytotoxic T cellTuberculosis PulmonaryAllelesCells CulturedGenetics (clinical)HLA-A AntigensbiologyMycobacterium tuberculosisFlow Cytometrybiology.organism_classificationVirologyMolecular biologyHLA-B Antigensbiology.proteinEpitope MappingCD8Genes & Immunity
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TAP-polymorphisms in juvenile onset psoriasis and psoriatic arthritis.

1996

Abstract Juvenile onset psoriasis is strongly associated with the HLA-class I genes Cw6 and B57 whereas patients with psoriatic arthritis show an increased frequency of HLA-B27. It is unclear whether additional major histocompatibility genes also increase disease susceptibility. The TAP genes (transporter associated with antigen processing) encode two membrane-spanning proteins that translocate antigenic peptides from the cytoplasm into the endoplasmic reticulum. Comparison of 60 patients with juvenile onset psoriasis, 63 psoriatic arthritis patients, and 101 caucasoid controls revealed an increase of the TAP1 ∗ 0101 allele in the psoriasis group, that could not be explained by linkage to o…

ImmunologyLinkage DisequilibriumMajor Histocompatibility ComplexPsoriatic arthritisATP Binding Cassette Transporter Subfamily B Member 3PsoriasismedicineImmunology and AllergyHumansPsoriasisAlleleATP Binding Cassette Transporter Subfamily B Member 2GenePolymorphism Geneticbiologybusiness.industryEndoplasmic reticulumArthritis PsoriaticHistocompatibility Antigens Class IGeneral MedicineTransporter associated with antigen processingHLA-DR Antigensmedicine.diseaseImmunologybiology.proteinTAP2ATP-Binding Cassette TransportersTAP1businessHuman immunology
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Major histocompatibility complex regulation of the class of the immune response: the H-2d haplotype determines poor interferon-γ response to several …

1990

The lymph node cells of CBA (H-2k), but not BALB/c (H-2d) mice, release interferon (IFN)-gamma into the supernatant when immunized with picryl chloride epicutaneously and then exposed to antigen (haptenized cells) in vitro 4 days later. The failure in IFN-gamma production maps to the major histocompatibility complex (MHC; H-2d) in the congenic BALB/c, BALB/k and BALB/b mice. The evidence that this is an MHC regulation of the class of response to a range of antigens and not a classical Ir gene effect is (a) the difference is seen with several antigens including picryl chloride, "oxazolone" and purified protein derivative of tuberculin and (b) BALB/c mice, which fail to produce IFN-gamma, sho…

ImmunologyMice Inbred StrainsDermatitis ContactMajor histocompatibility complexMajor Histocompatibility ComplexPicryl chlorideOxazoloneInterferon-gammaMicechemistry.chemical_compoundImmune systemH-2 AntigensAntigenInterferonmedicineAnimalsImmunology and AllergyInterferon gammaHistocompatibility Antigen H-2DbiologyH-2 AntigensImmunityHaplotypeschemistryImmunologybiology.proteinmedicine.drugEuropean Journal of Immunology
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Myxoma virus Leukemia-associated protein is responsible for major histocompatibility complex class I and Fas-CD95 down-regulation and defines scrapin…

2002

ABSTRACTDown-modulation of major histocompatibility class I (MHC-I) molecules is a viral strategy for survival in the host.Myxoma virus, a member of thePoxviridaefamily responsible for rabbit myxomatosis, can down-modulate the expression of MHC-I molecules, but the viral factor(s) has not been described. We cloned and characterized a gene coding for an endoplasmic reticulum (ER)-resident protein containing an atypical zinc finger and two transmembrane domains, which we called myxoma virus leukemia-associated protein (MV-LAP). MV-LAP down-regulated surface MHC-I and Fas-CD95 molecules upon transfection; the mechanism probably involves an exacerbation of endocytosis and was lost when the ER r…

ImmunologyMolecular Sequence DataDown-RegulationMyxoma virusReceptors Cell SurfaceMajor histocompatibility complexEndoplasmic ReticulumMicrobiologyVirusCell Line03 medical and health sciencesViral ProteinsMyxomatosis InfectiousVirologymedicineAnimalsFACTEUR VIRALPoxviridaeAGRONOMIEAmino Acid Sequencefas ReceptorComputingMilieux_MISCELLANEOUS030304 developmental biology[SDV.MP.VIR] Life Sciences [q-bio]/Microbiology and Parasitology/Virology0303 health sciencesBIOTECHNOLOGIEMyxomatosisbiologyBase SequenceVirulence030302 biochemistry & molecular biologyHistocompatibility Antigens Class IMyxoma virusMembrane ProteinsER retentionSequence Analysis DNAbiology.organism_classificationmedicine.diseaseVirology3. Good healthCTL*Lytic cycleInsect Science[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virologybiology.proteinPathogenesis and ImmunityReceptors VirusRabbitsT-Lymphocytes Cytotoxic
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Cross-Inhibition of Interferon-Induced Signals by GM-CSF Through a Block in Stat1 Activation

2007

We investigated the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) on biologic signals induced by interferon-alpha (IFN-alpha) and IFN-gamma. In hematopoietic cell lines, IFN-induced signaling was investigated by Western blotting, electrophoretic mobility shift assays (EMSA), flow cytometry, protein-tyrosine phosphatase (PTP) assays, and RT-PCR. GM-CSF inhibited IFN-alpha-induced and IFN-gamma-induced Stat1 tyrosine phosphorylation in a time-dependent manner. EMSA showed that GM-CSF inhibited IFN-alpha-induced and IFN-gamma-induced IFN-gamma activator sequence (GAS) binding activity. As a consequence, IFN-induced transcription of the early response gene, IFN-stimulated…

ImmunologyPhosphataseSuppressor of Cytokine Signaling ProteinsProtein tyrosine phosphataseBiologyCell Linechemistry.chemical_compoundVirologyGranulocyte Colony-Stimulating FactorHumansPhosphorylationHistocompatibility Antigens Class IGranulocyte-Macrophage Colony-Stimulating FactorTyrosine phosphorylationDNACell BiologyMolecular biologySTAT1 Transcription FactorIRF1chemistryTyrosine kinase 2PhosphorylationInterleukin-3InterferonsSignal transductionInterferon Regulatory Factor-1Signal TransductionTranscription FactorsProto-oncogene tyrosine-protein kinase SrcJournal of Interferon & Cytokine Research
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Impaired Th1 responses in mice deficient in Epstein-Barr virus-induced gene 3 and challenged with physiological doses of Leishmania major.

2005

Protection against Leishmania major is dependent on IL-12 release from L. major-infected dendritic cells (DC) that induce IFN-gamma-producing Th1/Tc1 cells. IL-27, a novel member of the IL-12 family, is a heterodimer composed of p28 and IL-12p40-related Epstein-Barr virus-induced gene 3 (EBI3), and was shown to be produced by DC. In this study, we utilized EBI3-deficient mice to investigate the role of IL-27 in leishmaniasis using physiological low-dose infections that mimic natural transmissions. Lesions in EBI3(-/-) mice were significantly larger between weeks 3 and 10 post infection, reaching up to approximately threefold increased lesion volumes compared to wild types. In parallel, derm…

ImmunologyPopulationCD11cLeishmaniasis CutaneousBiologyLesionMinor Histocompatibility AntigensMiceT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsLeishmania majorRNA MessengerReceptors CytokineeducationLeishmania majoreducation.field_of_studyEBI3Dendritic cellDendritic CellsTh1 Cellsbiology.organism_classificationImmunologyInterleukin 12Lymphmedicine.symptomEuropean journal of immunology
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