Search results for "Immunopathology"

showing 10 items of 155 documents

Benefits of immune protection versus immunopathology costs: a synthesis from cytokine KO models.

2017

5 pages; International audience; The inflammatory response can produce damage to host tissues and in several infectious diseases the most severe symptoms are due to immunopathology rather than a direct effect of pathogen multiplication. One hypothesis for the persistence of inflammatory damage posits that the benefits of protection towards infection outweigh the costs. We used data on knocked-out (KO) cytokine models [and the corresponding wild-type (WT) controls] to test this hypothesis. We computed differences in pathogen load and host survival between WT and KO and divided them by the WT values. Using this ratio provides an internal control for variation in pathogen species, host strain,…

0106 biological sciences0301 basic medicineMicrobiology (medical)medicine.medical_treatmentVirulenceInflammationImmunopathologyBiologyCommunicable Diseases010603 evolutionary biology01 natural sciencesMicrobiologyPersistence (computer science)Gene Knockout Techniques03 medical and health sciencesImmunopathologyGeneticsmedicine[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/SymbiosisAnimalsHumans[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMolecular BiologyPathogenCytokineEcology Evolution Behavior and SystematicsInflammationVirulenceHost (biology)Immune protectionHost survivalComputational BiologyPathogen loadDisease Models Animal030104 developmental biologyInfectious DiseasesCytokineHost-Pathogen InteractionsImmunologyCytokinesmedicine.symptom
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Immune activation increases susceptibility to oxidative tissue damage in Zebra Finches.

2006

Summary 1The innate immune response involves the production of highly reactive molecules (reactive oxygen and nitrogen species, ROS and RNS). These toxic compounds can effectively destroy invading pathogens but can also, non-specifically, target host cells. Tissue damage caused by ROS and RNS can be substantial if the inflammatory response is overactive, potentially inducing a so-called immunopathology. 2In this study, we induced an inflammatory response in Zebra Finches by the way of a LPS injection (lipopolysaccharide of the cell wall of Escherichia coli), using as a control a group of birds injected with saline (phosphate-buffered saline). Body mass was measured both before and 24 h afte…

0106 biological sciencesLipopolysaccharidefree radicals[ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyBiologymedicine.disease_cause010603 evolutionary biology01 natural sciencesimmune activation03 medical and health scienceschemistry.chemical_compoundImmune systemnitric oxideImmunopathologymedicine[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyimmunopathologyZebra finchEcology Evolution Behavior and SystematicsReactive nitrogen speciesComputingMilieux_MISCELLANEOUS030304 developmental biologyZebra Finchchemistry.chemical_classification0303 health sciencesReactive oxygen speciesInnate immune systemlipopolysaccharide[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biology3. Good healthchemistryImmunology[SDV.IMM]Life Sciences [q-bio]/ImmunologyOxidative stress
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Correlational selection on pro- and anti-inflammatory effectors.

2012

9 pages; International audience; Parasites impose a permanent threat for hosts. As a consequence, immune defenses are important for host fitness. However, the immune response can also produce self-damage and impair host fitness if not properly regulated. Effectors that up- and downregulate the immune response should, therefore, evolve in concert, and be under the action of correlational selection. To address this issue, we assessed the shape of the selection operating on pro- and anti-inflammatory effectors following an inflammatory challenge in laboratory mice. We found that selection acts on the combination of these two traits as individuals that produced large amount of pro-inflammatory …

0106 biological sciencesLipopolysaccharidesMale[ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunology01 natural sciencesMiceImmunopathologyDarwinian medicine[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/SymbiosisimmunopathologyGenetics0303 health sciencesEffectorFlow CytometryInterleukin-10Interleukin 10[SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunologyIL-10CytokinesRegression AnalysisFemalemedicine.symptomGeneral Agricultural and Biological Sciences[ SDV.MP.PAR ] Life Sciences [q-bio]/Microbiology and Parasitology/Parasitologymedicine.drug_classInflammationBiology010603 evolutionary biologysurvivalAnti-inflammatory03 medical and health sciencesImmune systemImmunityGeneticsmedicineEscherichia coliAnimals[SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologySelection GeneticEcology Evolution Behavior and SystematicsSelection (genetic algorithm)030304 developmental biologyIL-6[ SDE.BE ] Environmental Sciences/Biodiversity and Ecologyevolutionary immunologyInterleukin-6inflammationImmunology[SDE.BE]Environmental Sciences/Biodiversity and Ecology[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/SymbiosisEvolution; international journal of organic evolution
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Immunity and Virulence in Bird-Parasite Interactions.

2010

8 pages; International audience; The interaction between hosts and parasites is characterized by the evolution of reciproca adaptations aiming at reducing the cost of infection (from the host point of view) and to optimize host exploitation (from the parasite point of view). Within this co-evolutionary scenario, the immune system takes a central role. The immune system has evolved to fight off parasitic attacks. However, immune defences cannot be deployed without costs which set a limit to the protective effect of immunity. Moreover, immune defences impose strong selection pressures on the parasite and can favour the evolution of more virulent pathogen strains. In this article, we will disc…

0106 biological sciences[ SDV.MP.PAR ] Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyVirulenceBiology[ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunology010603 evolutionary biology01 natural sciencesimmune response03 medical and health sciencesImmune systemImmunityImmunopathology[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/SymbiosisParasite hostingimmunopathology[SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyPathogenCoevolution030304 developmental biology0303 health sciences[ SDE.BE ] Environmental Sciences/Biodiversity and EcologyHost (biology)biochemical phenomena metabolism and nutritioninfectionvirulence[SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunologyEvolutionary biologyImmunologybacteriaAnimal Science and Zoology[SDE.BE]Environmental Sciences/Biodiversity and Ecology[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/SymbiosisCoevolution
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IL-33/ST2 pathway drives regulatory T cell dependent suppression of liver damage upon cytomegalovirus infection.

2017

Regulatory T (Treg) cells dampen an exaggerated immune response to viral infections in order to avoid immunopathology. Cytomegaloviruses (CMVs) are herpesviruses usually causing asymptomatic infection in immunocompetent hosts and induce strong cellular immunity which provides protection against CMV disease. It remains unclear how these persistent viruses manage to avoid induction of immunopathology not only during the acute infection but also during life-long persistence and virus reactivation. This may be due to numerous viral immunoevasion strategies used to specifically modulate immune responses but also induction of Treg cells by CMV infection. Here we demonstrate that liver Treg cells …

0301 basic medicineCytomegalovirus InfectionCellular immunityViral DiseasesPhysiologyvirusesCytomegalovirusT-Lymphocytes RegulatoryMice0302 clinical medicineImmunopathologyImmune PhysiologyInterleukin-33 mouse ; mouse cytomegalovirus ; ST2 protein mouse ; T-lymphocytes regulatoryCellular typesCytotoxic T cellBiology (General)Immune ResponseImmunity CellularMice Inbred BALB CImmune cellsvirus diseasesRegulatory T cells3. Good healthmedicine.anatomical_structureInfectious DiseasesLiverCytomegalovirus InfectionsWhite blood cellsAnatomyBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.Signal TransductionResearch ArticleCell biologyBlood cellsQH301-705.5Regulatory T cellImmunologyT cellschemical and pharmacologic phenomenaCytotoxic T cellsBiologyResearch and Analysis MethodsMicrobiologyVirusCell Line03 medical and health sciencesImmune systemImmunityVirologyGeneticsmedicineAnimalsMolecular Biology TechniquesMolecular BiologyMedicine and health sciencesBiology and life sciencesBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.RC581-607Interleukin-33VirologyInterleukin-1 Receptor-Like 1 ProteinInterleukin 33Mice Inbred C57BL030104 developmental biologyAnimal cellsImmunologyParasitologyImmunologic diseases. AllergySpleen030215 immunologyCloningPLoS pathogens
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Microevolutionary response of a gut nematode to intestinal inflammation.

2017

7 pages; International audience; Parasitic helminths interfere with the immune response of their hosts to establish long-lasting, chronic infections. While favorable to the parasite, the capacity to dampen the immune response can also provide a benefit to the host in terms of reduced risk of immune disorders and immunopathology. The immunomodulatory role of nematodes has been exploited in clinical trials to treat a number of inflammatory and immune diseases. However, how parasites adapt to an inflammatory environment remains a poorly explored question. Here, we conducted a serial passage experiment where the gut nematode Heligmosomoides polygyrus was maintained for nine generations in mice …

0301 basic medicineGastrointestinal DiseasesInflammationHost-Parasite InteractionsRodent Diseases03 medical and health sciencesMice0302 clinical medicineImmune systemSerial passageImmunopathology[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/Symbiosismedicine[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyAnimalsAdaptationStrongylida InfectionsInflammationExperimental evolutionNematospiroides dubiusbiologyHost (biology)Life history traitsbiology.organism_classificationColitisBiological Evolution3. Good health030104 developmental biologyInfectious DiseasesNematodeExperimental evolutionImmunologybacteria[SDV.IMM]Life Sciences [q-bio]/ImmunologyParasitologyHeligmosomoides polygyrusmedicine.symptomSerial passage030215 immunology[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/Symbiosis
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Fate-Mapping of GM-CSF Expression Identifies a Discrete Subset of Inflammation-Driving T Helper Cells Regulated by Cytokines IL-23 and IL-1β.

2019

Summary Pathogenic lymphocytes initiate the development of chronic inflammatory diseases. The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) (encoded by Csf2) is a key communicator between pathogenic lymphocytes and tissue-invading inflammatory phagocytes. However, the molecular properties of GM-CSF-producing cells and the mode of Csf2 regulation in vivo remain unclear. To systematically study and manipulate GM-CSF+ cells and their progeny in vivo, we generated a fate-map and reporter of GM-CSF expression mouse strain (FROG). We mapped the phenotypic and functional profile of auto-aggressive T helper (Th) cells during neuroinflammation and identified the signature and pa…

0301 basic medicineMalemedicine.medical_treatmentImmunologyInterleukin-1betaInflammation610 Medicine & health10071 Functional Genomics Center ZurichBiology10263 Institute of Experimental Immunology03 medical and health sciencesInterferon-gammaMice0302 clinical medicineFate mappingImmunopathologymedicineInterleukin 23Immunology and AllergyAnimalsReceptorNeuroinflammationReceptors CXCR6InflammationMice KnockoutReceptors Interleukin-1 Type I2403 ImmunologyTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesReceptors InterleukinTh1 CellsPhenotype3. Good healthCell biology10040 Clinic for NeurologyMice Inbred C57BL030104 developmental biologyInfectious DiseasesCytokine030220 oncology & carcinogenesis2723 Immunology and AllergyInterleukin-23 Subunit p19570 Life sciences; biologyTh17 CellsFemalemedicine.symptomImmunity
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Context- and Tissue-Specific Regulation of Immunity and Tolerance by Regulatory T Cells

2016

The immune system has evolved to defend the organism against an almost infinite number of pathogens in a locally confined and antigen-specific manner while at the same time preserving tolerance to harmless antigens and self. Regulatory T (Treg) cells essentially contribute to an immunoregulatory network preventing excessive immune responses and immunopathology. There is emerging evidence that Treg cells not only operate in secondary lymphoid tissue but also regulate immune responses directly at the site of inflammation. Hence, the classification of Treg cells might need to be further extended by Treg cell subsets that are functionally and phenotypically polarized by their residency. In this…

0301 basic medicineRegulatory T cellFOXP3chemical and pharmacologic phenomenaContext (language use)InflammationBiology03 medical and health sciences030104 developmental biologymedicine.anatomical_structureImmune systemAntigenImmunityImmunopathologyImmunologymedicinemedicine.symptom
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Bronchial inflammation and bacterial load in stable COPD is associated with TLR4 overexpression.

2017

Toll-like receptors (TLRs) and nucleotide-binding oligomerisation domain (NOD)-like receptors (NLRs) are two major forms of innate immune sensors but their role in the immunopathology of stable chronic obstructive pulmonary disease (COPD) is incompletely studied. Our objective here was to investigate TLR and NLR signalling pathways in the bronchial mucosa in stable COPD.Using immunohistochemistry, the expression levels of TLR2, TLR4, TLR9, NOD1, NOD2, CD14, myeloid differentiation primary response gene 88 (MyD88), Toll-interleukin-1 receptor domain-containing adaptor protein (TIRAP), and the interleukin-1 receptor-associated kinases phospho-IRAK1 and IRAK4 were measured in the bronchial muc…

0301 basic medicineTIRAPMaleRespiratory SystemVital CapacityHAEMOPHILUS-INFLUENZAELUNG MICROBIOMEPathogenesisPulmonary Disease Chronic Obstructive0302 clinical medicineNOD2ImmunopathologyForced Expiratory VolumeNod1 Signaling Adaptor ProteinNOD1PhosphorylationCOPDSmoking11 Medical And Health SciencesMiddle AgedCPG-DNAbronchial inflammationAnti-Bacterial AgentsStreptococcus pneumoniaePseudomonas aeruginosaMOUSE LUNGFemaleLife Sciences & BiomedicineMoraxella catarrhalisSignal TransductionEXPRESSIONPulmonary and Respiratory MedicineCD14BronchiRespiratory MucosaReal-Time Polymerase Chain ReactionOBSTRUCTIVE PULMONARY-DISEASETLRs NLR bronchial inflammationNLRDENDRITIC CELL SUBSETS03 medical and health sciencesProtein DomainsmedicineHumansTLRsAgedTOLL-LIKE RECEPTORSCOPD TLR4InflammationScience & TechnologyBacteriabusiness.industrymedicine.diseaseHaemophilus influenzaeBacterial Loadrespiratory tract diseasesToll-Like Receptor 4TLR2030104 developmental biology030228 respiratory systemImmunologyINNATE IMMUNITYT-CELLSbusinessThe European respiratory journal
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Ammonium thiolactate and thiolactic acid: important hairdressers' allergens?

2002

030201 allergyAllergyThiolactic acidbusiness.industryDermatologymedicine.diseasemedicine.disease_cause030207 dermatology & venereal diseases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAllergenAmmonium thiolactatechemistryContact allergyImmunopathologyImmunologymedicineImmunology and AllergyOccupational exposurebusinessContact dermatitisContact Dermatitis
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