Search results for "Immune system"

showing 10 items of 2885 documents

Selective targeting of activated T cells in chronic intestinal inflammation

2009

Programmed cell death (apoptosis) has been implicated in normal biological processes as well as in the pathology of human diseases.1 The characterisation of genes involved in apoptosis has been pursued intensively and led to the identification of two major classes of genes: the bcl-2 family and the caspase family. Caspases are proteases that cleave their target substrates at specific peptide sequences and during apoptosis the activation of caspases takes place in a cascade fashion, leading to nuclear engulfment and cell death. Thus, caspases represent key functional components of the apoptosis pathway in human cells. Resistance against apoptosis is a key phenomenon in various chronic inflam…

Programmed cell deathRecombinant Fusion ProteinsT-LymphocytesT cellApoptosisLymphocyte ActivationProinflammatory cytokineImmune systemmedicineAnimalsHumansIntestinal MucosaCaspasebiologyCaspase 3Intrinsic apoptosisGastroenterologyColitisCell biologymedicine.anatomical_structureApoptosisChronic DiseaseModels Animalbiology.proteinInterleukin-2Tumor necrosis factor alphaGut
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Human parvovirus B19 induced apoptotic bodies contain altered self-antigens that are phagocytosed by antigen presenting cells.

2013

Human parvovirus B19 (B19V) from the erythrovirus genus is known to be a pathogenic virus in humans. Prevalence of B19V infection has been reported worldwide in all seasons, with a high incidence in the spring. B19V is responsible for erythema infectiosum (fifth disease) commonly seen in children. Its other clinical presentations include arthralgia, arthritis, transient aplastic crisis, chronic anemia, congenital anemia, and hydrops fetalis. In addition, B19V infection has been reported to trigger autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. However, the mechanisms of B19V participation in autoimmunity are not fully understood. B19V induced chronic dise…

Programmed cell deathScienceAntigen-Presenting CellsArthritisApoptosisAutoimmunitySpodopteraViral Nonstructural ProteinsBiologymedicine.disease_causeAutoantigensVirusautoimmuniteettiImmune toleranceAutoimmunityParvoviridae InfectionsPathogenesis03 medical and health sciences0302 clinical medicineImmune systemPhagocytosisImmune ToleranceParvovirus B19 HumanSf9 CellsHuman Parvovirus B19medicineta319AnimalsHumansAntigen-presenting cellself-antigens030304 developmental biology0303 health sciencesMultidisciplinaryQta1182RHep G2 CellsFlow Cytometrymedicine.diseaseVirology3. Good healthImmunologyMicroscopy Electron ScanningMedicineResearch Article030215 immunologyPLoS ONE
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Autophagy-Dependent Anticancer Immune Responses Induced by Chemotherapeutic Agents in Mice

2011

Antineoplastic chemotherapies are particularly efficient when they elicit immunogenic cell death, thus provoking an anticancer immune response. Here we demonstrate that autophagy, which is often disabled in cancer, is dispensable for chemotherapy-induced cell death but required for its immunogenicity. In response to chemotherapy, autophagy-competent, but not autophagy-deficient, cancers attracted dendritic cells and T lymphocytes into the tumor bed. Suppression of autophagy inhibited the release of adenosine triphosphate (ATP) from dying tumor cells. Conversely, inhibition of extracellular ATP-degrading enzymes increased pericellular ATP in autophagy-deficient tumors, reestablished the recr…

Programmed cell deathcells cancer immunogenicity calreticulin exposure hmgb1Antineoplastic AgentsBiologyimmunogenicityNOMicechemistry.chemical_compoundAdenosine TriphosphateImmune systemCell Line TumorNeoplasmsAutophagyExtracellularAnimalsHumanscancerMice Inbred BALB CMultidisciplinaryCell DeathImmunogenicityAutophagyDendritic CellsMice Inbred C57BLhmgb1chemistryCell cultureCancer researchImmunogenic cell deathcellsMitoxantroneCalreticulinAdenosine triphosphatecalreticulin exposure
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T cell-independent joint destruction

1998

Rheumatoid Arthritis (RA) is a chronic systemic disorder of unknown etiology. Although, early and late stages of the disease may be driven by different processes, affected joints are characterized by inflammation, synovial hyperplasia, and abnormal immune responses [1]. The abundance of T cells within the rheumatoid synovium as well as the association of certain major histocompatibility complex (MHC) class II molecules with RA [2] implied a central role for T cells in the pathophysiology of the disease. However, recent advances in molecular biology have fostered new concepts for the pathogenesis of RA. Specifically, the investigation of early stages of disease, the development of novel anim…

Property (philosophy)media_common.quotation_subjectT cellInflammationDiseaseBiologyMajor histocompatibility complexExperiential learningExistentialismPathogenesisMode (music)Immune systemPerceptionSynovitismedicineRelation (history of concept)media_commonTime perceptionmedicine.diseasemedicine.anatomical_structureRheumatoid arthritisImmunologySpitebiology.proteinmedicine.symptomPsychologyCognitive psychology
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Immune depression induced by acanthocephalan parasites in their intermediate crustacean host: consequences for the risk of super-infection and links …

2009

9 pages; International audience; Parasite survival in hosts mainly depends on the capacity to circumvent the host immune response. Acanthocephalan infections in gammarids are linked with decreased activity of the prophenoloxidase (ProPO) system, suggesting an active immunosuppression process. Nevertheless, experimental evidence for this hypothesis is lacking: whether these parasites affect several immune pathways is unknown and the consequences of such immune change have not been investigated. In particular, the consequences for other pathogens are not known; neither are the links with other parasite-induced manipulations of the host. Firstly, using experimental infections of Pomphorhynchus…

ProphenoloxidaseMaleImmune depression[ SDV.MP.PAR ] Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyHemocytesCyprinidaeBiology[ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunologyAcanthocephalanAcanthocephalaHost-Parasite InteractionsBehavioural manipulationFish DiseasesImmune systemImmunityCrustacea[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/SymbiosisParasite hostingAnimalsGammaridEnzyme PrecursorsHost (biology)Intermediate hostHaemocytebiology.organism_classificationGammarus pulexInfectious DiseasesImmunologyParasitologyPomphorhynchus laevisFemaleImmunocompetenceImmunocompetenceCatechol OxidaseInternational journal for parasitology
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Proteasomes shape the repertoire of T cells participating in antigen-specific immune responses

2006

Differences in the cleavage specificities of constitutive proteasomes and immunoproteasomes significantly affect the generation of MHC class I ligands and therefore the activation of CD8-positive T cells. Based on these findings, we investigated whether proteasomal specificity also influences CD8-positive T cells during thymic selection by peptides derived from self proteins. We find that one of the self peptides responsible for positive selection of ovalbumin-specific OT-1 T cells, which is derived from the f-actin capping protein (Cpalpha1), is efficiently generated only by immunoproteasomes. Furthermore, OT-1 mice backcrossed onto low molecular mass protein 7 (LMP7)-deficient mice show a…

Proteasome Endopeptidase ComplexOvalbuminActin Capping ProteinsT-LymphocytesMolecular Sequence DataReceptors Antigen B-CellThymus GlandBiologyEpitopeInterleukin 21MiceImmune systemAntigenMultienzyme ComplexesMHC class ICytotoxic T cellT cell repertoire; selectionAnimalsIL-2 receptorAmino Acid SequenceAntigensSelection GeneticBone Marrow TransplantationMice KnockoutMultidisciplinaryBiological SciencesMolecular biologyPeptide FragmentsMice Inbred C57BLCTL*biology.proteinLymph Nodes
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Conversion of crustacean hemocyanin to catecholoxidase

2004

Crustacean hemocyanin as oxygen carrier and catecholoxidase as enzymes belong to the same protein family (type 3 copper proteins) sharing very similar active sites. Treatment with SDS of these hemocyanins results in an opening of the entrance to the active site for bulky phenolic compounds. This demonstrates, that almost all hemocyanin subunits possess the ability of catecholoxidase activity.

Protein familyCopper proteinTyrosinasemedicine.medical_treatmentGeneral Physics and Astronomychemistry.chemical_elementchemical and pharmacologic phenomenacomplex mixturesOxygenStructural BiologyCrustaceamedicineAnimalsGeneral Materials ScienceCatechol oxidasechemistry.chemical_classificationbiologyActive sitehemic and immune systemsHemocyaninCell BiologyEnzymechemistryBiochemistryHemocyaninsbiology.proteinCatechol OxidaseMicron
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Distinct endocytic recycling of myelin proteins promotes oligodendroglial membrane remodeling.

2008

The central nervous system myelin sheath is a multilayered specialized membrane with compacted and non-compacted domains of defined protein composition. How oligodendrocytes regulate myelin membrane trafficking and establish membrane domains during myelination is largely unknown. Oligodendroglial cells respond to neuronal signals by adjusting the relative levels of endocytosis and exocytosis of the major myelin protein, proteolipid protein (PLP). We investigated whether endocytic trafficking is common to myelin proteins and analyzed the endocytic fates of proteins with distinct myelin subdomain localization. Interestingly, we found that PLP, myelin-associated glycoprotein (MAG) and myelin-o…

Proteolipid protein 1Endocytic cycleCell MembraneEndocytic recyclingCell BiologyBiologyEndocytosisExocytosisEndocytosisCell biologyMyelin oligodendrocyte glycoproteinMyelinMiceMyelin-Associated GlycoproteinOligodendrogliamedicine.anatomical_structurenervous systemimmune system diseasesCompact myelinmedicinebiology.proteinAnimalsMyelin-Oligodendrocyte GlycoproteinMyelin Proteolipid ProteinMyelin ProteinsJournal of cell science
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Perturbed interactions of mutant proteolipid protein/DM20 with cholesterol and lipid rafts in oligodendroglia: implications for dysmyelination in spa…

2006

Missense mutations in the humanPLP1gene lead to dysmyelinating diseases with a broad range of clinical severity, ranging from severe Pelizaeus–Merzbacher disease (PMD) to milder spastic paraplegia type 2 (SPG-2). The molecular pathology has been generally attributed to endoplasmic reticulum (ER) retention of misfolded proteolipid protein (PLP) (and its splice isoform DM20) and induction of the unfolded protein response. As opposed to previous studies of heterologous expression systems, we have analyzed PLP/DM20 trafficking in oligodendroglial cells, thereby revealing differences between PMD and SPG-2-associated PLP/DM20 isoforms. PLPA242Vand DM20A242V(jimpy-msdin mice), associated with seve…

Proteolipid protein 1Time FactorsLeupeptinsBlotting WesternGene Expressionchemical and pharmacologic phenomenaNerve Tissue ProteinsBiologyProtein degradationCysteine Proteinase InhibitorsTransfectionMiceMice Neurologic MutantsCricetulusMembrane MicrodomainsMutant proteinimmune system diseasesCricetinaeAnimalsImmunoprecipitationMyelin Proteolipid ProteinLipid raftCells CulturedGeneral NeuroscienceEndoplasmic reticulumCholesterol bindingER retentionArticlesImmunohistochemistryCell biologynervous system diseasesOligodendrogliaProtein TransportCholesterolBiochemistryUnfolded protein responselipids (amino acids peptides and proteins)Mutant ProteinsSubcellular FractionsThe Journal of neuroscience : the official journal of the Society for Neuroscience
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Human CD4+CD25+ regulatory T cells: proteome analysis identifies galectin-10 as a novel marker essential for their anergy and suppressive function.

2007

AbstractCD4+CD25+Foxp3+ regulatory T cells (CD25+ Treg cells) direct the maintenance of immunological self-tolerance by active suppression of autoaggressive T-cell populations. However, the molecules mediating the anergic state and regulatory function of CD25+ Treg cells are still elusive. Using differential proteomics, we identified galectin-10, a member of the lectin family, as constitutively expressed in human CD25+ Treg cells, while they are nearly absent in resting and activated CD4+ T cells. These data were confirmed on the mRNA and protein levels. Single-cell staining and flow cytometry showed a strictly intracellular expression of galectin-10 in CD25+ Treg cells. Specific inhibition…

ProteomeGalectinsImmunologychemical and pharmacologic phenomenaBiologyBiochemistryT-Lymphocytes RegulatoryFlow cytometrymedicineHumansIL-2 receptorCells CulturedGalectinCell ProliferationClonal AnergyMessenger RNAmedicine.diagnostic_testFOXP3Antibodies Monoclonalhemic and immune systemsForkhead Transcription FactorsCell BiologyHematologyCell biologySelf ToleranceGene Expression RegulationProteomeImmunologyIntracellularFunction (biology)BiomarkersBlood
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