Search results for "cept"

showing 10 items of 15508 documents

Clr-a: A Novel Immune-Related C-Type Lectin-like Molecule Exclusively Expressed by Mouse Gut Epithelium

2017

Abstract The mouse gut epithelium represents a constitutively challenged environment keeping intestinal commensal microbiota at bay and defending against invading enteric pathogens. The complex immunoregulatory network of the epithelial barrier surveillance also involves NK gene complex (NKC)–encoded C-type lectin-like molecules such as NKG2D and Nkrp1 receptors. To our knowledge, in this study, we report the first characterization of the orphan C-type lectin-like molecule Clr-a encoded by the Clec2e gene in the mouse NKC. Screening of a panel of mouse tissues revealed that Clec2e transcripts are restricted to the gastrointestinal tract. Using Clr-a–specific mAb, we characterize Clr-a as a …

0301 basic medicineImmunoblottingImmunologyCryptFluorescent Antibody TechniqueCell SeparationBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationC-type lectinAnimalsImmunology and AllergyLectins C-TypeIntestinal MucosaReceptorMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionFlow CytometryNKG2DIntestinal epitheliumMolecular biologyGut EpitheliumMice Inbred C57BLImmunosurveillance030104 developmental biology030215 immunologyThe Journal of Immunology
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EBI2 in splenic and local immune responses and in autoimmunity

2017

Abstract The seven transmembrane G protein-coupled receptor EBV-induced gene 2 (EBI2), also known as GPR183, is expressed in particular in immune cells. Activated by its endogenous ligands, which are a group of oxysterols, it functions as a chemo-attractant receptor, mediating cell migration. In coordination with other receptors, EBI2 plays important roles in controlling the migration of immune cells during the course of a T-dependent Ab response in the spleen. In recent years, it has become clear that EBI2 also has other roles to play in the immune system. Thus, EBI2 seems to be involved in innate immune responses, such as those mediated by TLR signaling, and it has been implicated in regi…

0301 basic medicineImmunologyAutoimmunitySpleenBiologymedicine.disease_causeReceptors G-Protein-CoupledAutoimmunity03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsHumansImmunology and AllergyReceptorG protein-coupled receptorInnate immune systemGPR183Cell migrationCell Biologybiochemical phenomena metabolism and nutritionImmunity Innate030104 developmental biologymedicine.anatomical_structureImmunologybacteriaSpleen030217 neurology & neurosurgeryJournal of Leukocyte Biology
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Targeting cellular fatty acid synthesis limits T helper and innate lymphoid cell function during intestinal inflammation and infection

2019

CD4+ T cells contribute critically to a protective immune response during intestinal infections, but have also been implicated in the aggravation of intestinal inflammatory pathology. Previous studies suggested that T helper type (Th)1 and Th17 cells depend on de novo fatty acid (FA) synthesis for their development and effector function. Here, we report that T-cell-specific targeting of the enzyme acetyl-CoA carboxylase 1 (ACC1), a major checkpoint controlling FA synthesis, impaired intestinal Th1 and Th17 responses by limiting CD4+ T-cell expansion and infiltration into the lamina propria in murine models of colitis and infection-associated intestinal inflammation. Importantly, pharmacolog…

0301 basic medicineImmunologyBiologyMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemRAR-related orphan receptor gammamedicineAnimalsImmunology and AllergyFatty acid synthesisBarrier functionLamina propriaEffectorFatty AcidsInnate lymphoid cellT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3ColitisInflammatory Bowel DiseasesImmunity InnateBiosynthetic PathwaysDisease Models Animal030104 developmental biologymedicine.anatomical_structurechemistryImmunologyLipogenesisBiomarkersAcetyl-CoA Carboxylase030215 immunologyMucosal Immunology
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Rheostatic Functions of Mast Cells in the Control of Innate and Adaptive Immune Responses

2017

Mast cells are evolutionarily ancient cells, endowed with a unique developmental, phenotypic, and functional plasticity. They are resident cells that participate in tissue homeostasis by constantly sampling the microenvironment. As a result of their large repertoire of receptors, they can respond to multiple stimuli and selectively release different types and amounts of mediator. Here, we present and discuss the recent mast cell literature, focusing on studies that demonstrate that mast cells are more than a switch that is turned ‘off’ when in the resting state and ‘on’ when in the degranulating state. We propose a new vision of mast cells in which, by operating in a ‘rheostatic 

0301 basic medicineImmunologyBiologymedicine.disease_causeAutoimmunityImmunomodulation03 medical and health sciencesMediatorImmune systemImmunityMAST CELLmedicineAnimalsHomeostasisHumansADAPTIVE IMMUNITYImmunology and AllergyMast CellsReceptorTissue homeostasisImmunology and Allergy; ImmunologyMAST CELL INNATE IMMUNITY ADAPTIVE IMMUNITYMast cellAcquired immune systemImmunity InnateCell biologySelf Tolerance030104 developmental biologymedicine.anatomical_structureCellular MicroenvironmentOrgan SpecificityImmunologyINNATE IMMUNITYTrends in Immunology
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Extravascular coagulation in hematopoietic stem and progenitor cell regulation

2018

Abstract The hemostatic system plays pivotal roles in injury repair, innate immunity, and adaptation to inflammatory challenges. We review the evidence that these vascular-protective mechanisms have nontraditional roles in hematopoietic stem cell (HSC) maintenance in their physiological bone marrow (BM) niches at steady-state and under stress. Expression of coagulation factors and the extrinsic coagulation initiator tissue factor by osteoblasts, tissue-resident macrophages, and megakaryocytes suggests that endosteal and vascular HSC niches are functionally regulated by extravascular coagulation. The anticoagulant endothelial protein C receptor (EPCR; Procr) is highly expressed by primitive …

0301 basic medicineImmunologyBone Marrow Cells030204 cardiovascular system & hematologyBiologyThrombomodulinBiochemistry03 medical and health sciences0302 clinical medicineBone MarrowStress PhysiologicalmedicineAnimalsHumansThromboplastinStem Cell NicheProgenitor cellBlood CoagulationEndothelial protein C receptorReview SeriesHematopoietic Stem Cell TransplantationHematopoietic stem cellCell DifferentiationCell BiologyHematologyHematopoietic Stem CellsHematopoiesisCell biologyHaematopoiesis030104 developmental biologymedicine.anatomical_structureStem cellBiomarkersFibrinolytic agentSignal TransductionBlood
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Danger signals: Chemotherapy enhancers?

2017

IF 9.614; International audience; Endogenous danger signals are molecules normally present in a given cell compartment that are rapidly released following cell stress and induce immune responses. We and others have shown that dying tumor cells treated with some chemotherapies are able to induce anticancer immune responses, which rely on their release of danger signals such as the nuclear protein HMGB1. DNA can also be released from chemotherapy-treated tumor cells, act as a danger signal, and boost anticancer immunity. While the immunostimulatory properties of DNA have been identified for decades, the recent discovery of a novel family of receptors, cytosolic DNA sensors, has provided a nov…

0301 basic medicineImmunologyCelleducationBiologyHMGB1CD8+ T cellschemotherapyCancer Vaccines03 medical and health sciences0302 clinical medicineImmune systemDrug TherapyNeoplasmsmedicineImmunology and AllergyCytotoxic T cellAnimalsHumanscancer[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMolecular Targeted TherapyNuclear proteinHMGB1 ProteinReceptorinnate immunityInnate immune systemDNAadaptive immunityAcquired immune systemCombined Modality TherapyImmunity Innate3. Good health030104 developmental biologymedicine.anatomical_structureImmunologybiology.proteinCancer research[SDV.IMM]Life Sciences [q-bio]/ImmunologyImmunotherapy030215 immunologySignal TransductionSTINGImmunological Reviews
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NKG2D stimulation of CD8(+) T cells during priming promotes their capacity to produce cytokines in response to viral infection in mice

2017

NKG2D is an activating receptor that is expressed on most cytotoxic cells of the immune system, including NK cells, γδ and CD8+ T cells. It is still a matter of debate whether and how NKG2D mediates priming of CD8+ T cells in vivo, due to a lack of studies where NKG2D is eliminated exclusively in these cells. Here we studied the impact of NKG2D on effector CD8+ T-cell formation. NKG2D-deficiency that is restricted to murine CD8+ T cells did not impair antigen-specific T-cell expansion following mCMV and LCMV infection, but reduced their capacity to produce cytokines. Upon infection, conventional dendritic cells induce NKG2D ligands, which drive cytokine production on CD8+ T cells via the Da…

0301 basic medicineImmunologyCytokines ; Dap10 ; Effector CD8+ T cells ; LCMV ; NKG2D ; mCMVchemical and pharmacologic phenomenaBiologyCD8+ T cellsNKG2D03 medical and health sciencesInterleukin 21Immunology and AllergyCytotoxic T cellIL-2 receptorAntigen-presenting cellZAP70BIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.hemic and immune systemsNKG2DNatural killer T cellmCMVbiological factors3. Good health030104 developmental biologyCostimulationPrimingImmunologyInterleukin 12CytokinesBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.European journal of immunology
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Donor interleukin-22 and host type I interferon signaling pathway participate in intestinal graft-versus-host disease via STAT1 activation and CXCL10.

2014

Acute graft-versus-host disease (aGVHD) remains a major complication following allogeneic hematopoietic cell transplantation, limiting the success of this therapy. We previously reported that interleukin-22 (IL-22) participates to aGVHD development, but the underlying mechanisms of its contribution remain poorly understood. In this study, we analyzed the mechanism of the pathological function of IL-22 in intestinal aGVHD. Ex-vivo colon culture experiments indicated that IL-22 was able to induce Th1-like inflammation via signal transducer and activator of transcription factor-1 (STAT1) and CXCL10 induction in the presence of type I interferon (IFN). To evaluate a potential synergy between IL…

0301 basic medicineImmunologyGraft vs Host DiseaseInflammationReceptor Interferon alpha-betaInterleukin 2203 medical and health sciencesMiceInterferonimmune system diseasesBone MarrowmedicineImmunology and AllergyCXCL10AnimalsTransplantation HomologousHumansSTAT1Intestine LargeIntestinal MucosaBone Marrow TransplantationMice KnockoutMice Inbred BALB CbiologyInterleukinsTh1 CellsTissue DonorsTransplantationMice Inbred C57BLChemokine CXCL10030104 developmental biologymedicine.anatomical_structuresurgical procedures operativeSTAT1 Transcription FactorGene Expression RegulationHematologic NeoplasmsImmunologyInterferon Type Ibiology.proteinSTAT proteinBone marrowmedicine.symptomWhole-Body Irradiationmedicine.drugSignal Transduction
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TLR4 participates in the transmission of ethanol-induced neuroinflammation via astrocyte-derived extracellular vesicles

2019

Background Current evidence indicates that extracellular vesicles (EVs) participate in intercellular signaling, and in the regulation and amplification of neuroinflammation. We have previously shown that ethanol activates glial cells through Toll-like receptor 4 (TLR4) by triggering neuroinflammation. Here, we evaluate if ethanol and the TLR4 response change the release and inflammatory content of astrocyte-derived EVs, and whether these vesicles are capable of communicating with neurons by spreading neuroinflammation. Methods Cortical neurons and astrocytes in culture were used. EVs were isolated from the extracellular medium of the primary culture of the WT and TLR4-KO astrocytes treated …

0301 basic medicineImmunologyInflammationlcsh:RC346-42903 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineWestern blotNeuroinflammationGlial cellsExtracellularmedicineAnimalsProtein Interaction MapsReceptorNeuroinflammationCells Culturedlcsh:Neurology. Diseases of the nervous systemInflammationMice KnockoutNeuronsmedicine.diagnostic_testEthanolChemistryGeneral NeuroscienceResearchExtracellular vesiclesCell biologyMice Inbred C57BLToll-Like Receptor 4030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesTLR4medicine.symptom030217 neurology & neurosurgeryIntracellularAstrocyteJournal of Neuroinflammation
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Frontline Science: Mast cells regulate neutrophil homeostasis by influencing macrophage clearance activity

2019

Abstract The receptor tyrosine kinase cKit and its ligand stem cell factor are essential for mast cells (MC) development and survival. Strains with mutations affecting the Kit gene display a profound MC deficiency in all tissues and have been extensively used to investigate the role of MC in both physiologic and pathologic conditions. However, these mice present a variety of abnormalities in other immune cell populations that can affect the interpretation of MC-related responses. C57BL/6 KitW-sh are characterized by an aberrant extramedullary myelopoiesis and systemic neutrophilia. MC deficiency in KitW-sh mice can be selectively repaired by engraftment with in vitro-differentiated MC to va…

0301 basic medicineImmunologyKit (W-sh) mice; macrophages; mast cell; neutrophils; phagocytosisBone Marrow CellsCell CountStem cell factormacrophageReceptor tyrosine kinase03 medical and health sciences0302 clinical medicineImmune systemneutrophilsGranulocyte Colony-Stimulating FactormedicineAnimalsHomeostasisImmunology and AllergyMacrophageMyeloid CellsMast CellsNeutrophil homeostasisCD11b AntigenNeutrophil clearancebiologyInterleukin-17neutrophilphagocytosisCell BiologyKit (W-sh) miceNeutrophiliaHematopoiesismacrophagesCell biologyMice Inbred C57BLProto-Oncogene Proteins c-kitPhenotype030104 developmental biologybiology.proteinCytokinesInflammation Mediatorsmedicine.symptommast cellEx vivoSignal Transduction030215 immunologyJournal of Leukocyte Biology
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