Search results for "IMMUNOLOGY"

showing 10 items of 9651 documents

Thymus-derived regulatory T cells are positively selected on natural self-antigen through cognate interactions of high functional avidity

2016

Regulatory T (Treg) cells expressing Foxp3 transcripton factor are essential for immune homeostasis. They arise in the thymus as a separate lineage from conventional CD4+Foxp3- T (Tconv) cells. Here, we show that the thymic development of Treg cells depends on the expression of their endogenous cognate self-antigen. The formation of these cells was impaired in mice lacking this self-antigen, while Tconv cell development was not negatively affected. Thymus-derived Treg cells were selected by self-antigens in a specific manner, while autoreactive Tconv cells were produced through degenerate recognition of distinct antigens. These distinct modes of development were associated with the expressi…

0301 basic medicineCell typeCancer ResearchEncephalomyelitis Autoimmune ExperimentalMultiple Sclerosis[SDV]Life Sciences [q-bio]ImmunologyReceptors Antigen T-CellEndogenyT-Cell Antigen Receptor Specificitychemical and pharmacologic phenomenaThymus GlandBiologymedicine.disease_causeAutoantigensT-Lymphocytes RegulatoryAutoimmunity03 medical and health sciencesMice0302 clinical medicineAntigenT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsHumansAvidityCTLA-4 AntigenReceptorClonal Selection Antigen-MediatedCells CulturedMice KnockoutCell growthFOXP3Forkhead Transcription Factorshemic and immune systemsPeptide Fragments[SDV] Life Sciences [q-bio]Mice Inbred C57BL030104 developmental biologyInfectious DiseasesImmunologyMyelin-Oligodendrocyte Glycoprotein030215 immunology
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Mast cells crosstalk with B cells in the gut and sustain IgA response in the inflamed intestine.

2021

B lymphocytes are among the cell types whose effector functions are modulated by mast cells (MCs). The B/MC crosstalk emerged in several pathological settings, notably the colon of inflammatory bowel disease (IBD) patients is a privileged site in which MCs and IgA+ cells physically interact. Herein, by inducing conditional depletion of MCs in red MC and basophil (RMB) mice, we show that MCs control B cell distribution in the gut and IgA serum levels. Moreover, in dextran sulfate sodium (DSS)-treated RMB mice, the presence of MCs is fundamental for the enlargement of the IgA+ population in the bowel and the increase of systemic IgA production. Since both conventional B-2 and peritoneal-deriv…

0301 basic medicineCell typeColon[SDV]Life Sciences [q-bio]ImmunologyPopulationInflammationBasophilBiologySettore MED/08 - Anatomia Patologicabehavioral disciplines and activitiesInflammatory bowel diseasecell-to-cell interplay colitis IgAinnate-like B cells mast cells03 medical and health sciencesMice0302 clinical medicinemedicineImmunology and AllergyAnimalsMast CellsColitisIntestinal MucosaeducationB cellComputingMilieux_MISCELLANEOUSInflammationeducation.field_of_studyB-LymphocytesTumor Necrosis Factor-alphaDextran Sulfatemedicine.diseaseColitisInflammatory Bowel DiseaseshumanitiesInnate-like B cellsGastrointestinal MicrobiomeImmunoglobulin AMice Inbred C57BLCrosstalk (biology)030104 developmental biologymedicine.anatomical_structureCell-to-cell interplayCell-to-cell interplay; Colitis; IgA; Innate-like B cells; Mast cellsImmunologymedicine.symptomIgA030215 immunologyEuropean journal of immunologyReferences
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Cell-Type-Specific Responses to Interleukin-1 Control Microbial Invasion and Tumor-Elicited Inflammation in Colorectal Cancer.

2017

Summary Chronic inflammation drives the progression of colorectal cancer (CRC). Increased expression of interleukin (IL)-17A is associated with poor prognosis, and IL-17A blockade curbs tumor progression in preclinical models of CRC. Here we examined the impact of IL-1 signaling, a key regulator of the IL-17 pathway, in different cell types within the CRC microenvironment. Genetic deletion of the IL-1 receptor (IL-1R1) in epithelial cells alleviated tumorigenesis in the APC model of CRC, demonstrating a cell-autonomous role for IL-1 signaling in early tumor seed outgrowth. T cell specific ablation of IL-1R1 decreased tumor-elicited inflammation dependent on IL-17 and IL-22, thereby reducing…

0301 basic medicineCell typeColorectal cancerCarcinogenesisNeutrophilsmedicine.medical_treatmentImmunologyMedizinInflammationBiologymedicine.disease_causeArticle03 medical and health sciencesMice0302 clinical medicineSalmonellamedicineTumor MicroenvironmentImmunology and AllergyAnimalsHumansCells CulturedInflammationMice KnockoutTumor microenvironmentSalmonella Infections AnimalInterleukinsInterleukin-17InterleukinReceptors Interleukin-1medicine.disease030104 developmental biologyInfectious DiseasesCytokineTumor progressionOrgan Specificity030220 oncology & carcinogenesisCancer researchmedicine.symptomCarcinogenesisColorectal NeoplasmsInterleukin-1Signal TransductionImmunity
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Epithelium‐specific MyD88 signaling, but not DCs or macrophages, control acute intestinal infection with Clostridium difficile

2019

Infection with Clostridium difficile is one of the major causes of health care acquired diarrhea and colitis. Signaling though MyD88 downstream of TLRs is critical for initiating the early protective host response in mouse models of C. difficile infection (CDI). In the intestine, MyD88 is expressed in various tissues and cell types, such as the intestinal epithelium and mononuclear phagocytes (MNP), including DC or macrophages. Using a genetic gain-of-function system, we demonstrate here that restricting functional MyD88 signaling to the intestinal epithelium, but also to MNPs is sufficient to protect mice during acute CDI by upregulation of the intestinal barrier function and recruitment o…

0301 basic medicineCell typeImmunologyBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationmedicineAnimalsImmunology and AllergyIntestinal MucosaColitisEnterocolitis PseudomembranousBarrier functionClostridioides difficileMacrophagesDendritic CellsClostridium difficilemedicine.diseaseIntestinal epitheliumPhenotypeEpitheliumDisease Models Animal030104 developmental biologymedicine.anatomical_structureHost-Pathogen InteractionsMyeloid Differentiation Factor 88ImmunologySignal Transduction030215 immunologyEuropean Journal of Immunology
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NF-κB-inducing kinase is essential for B-cell maintenance in mice

2015

NF-κB-inducing kinase (NIK) is a key mediator of the noncanonical NF-κB signaling pathway, which is critical for normal B-cell development and function. It is well established that the complete deletion of NIK in mice results in defective B cells and impaired secondary lymphoid organogenesis. To address the role of NIK deficiency specifically in B cells, we generated a new mouse strain for the conditional deletion of this kinase. Deletion of NIK during B-cell development results in a drastic reduction of mature B cells from the transitional 2 stage on, while B-1 B cells are less affected. Moreover, deletion of NIK in the germinal centers decreases the numbers of germinal center B cells and …

0301 basic medicineCell typeKinaseImmunologyGerminal centerOrganogenesisBiologyCell biology03 medical and health sciences030104 developmental biologymedicine.anatomical_structureMediatorImmunoglobulin class switchingImmunologymedicineImmunology and AllergySignal transductionB cellEuropean Journal of Immunology
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Signalling strength determines proapoptotic functions of STING

2017

Mammalian cells use cytosolic nucleic acid receptors to detect pathogens and other stress signals. In innate immune cells the presence of cytosolic DNA is sensed by the cGAS–STING signalling pathway, which initiates a gene expression programme linked to cellular activation and cytokine production. Whether the outcome of the STING response varies between distinct cell types remains largely unknown. Here we show that T cells exhibit an intensified STING response, which leads to the expression of a distinct set of genes and results in the induction of apoptosis. Of note, this proapoptotic STING response is still functional in cancerous T cells and delivery of small molecule STING agonists prev…

0301 basic medicineCell typeLeukemia T-CellTranscription Geneticmedicine.medical_treatmentScienceCellsT-LymphocytesGeneral Physics and AstronomyActivationApoptosisInnate Immune SensorBiologyCytosolic DnaCgasGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesCyclic Gmp-Amp[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicineAnimalsReceptorlcsh:ScienceMultidisciplinaryInnate immune systemEffectorQ2nd-MessengerMembrane ProteinsGeneral ChemistryHedgehog signaling pathwayeye diseases3. Good healthCell biologyMice Inbred C57BLSting030104 developmental biologyCytokineDi-GmpImmunologylcsh:QInterferon Regulatory Factor-3Signal transductionTumor Suppressor Protein p53InfectionProtein BindingSignal TransductionNature Communications
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Taking Advantage of Nature’s Gift: Can Endogenous Neural Stem Cells Improve Myelin Regeneration?

2016

Irreversible functional deficits in multiple sclerosis (MS) are directly correlated to axonal damage and loss. Neurodegeneration results from immune-mediated destruction of myelin sheaths and subsequent axonal demyelination. Importantly, oligodendrocytes, the myelinating glial cells of the central nervous system, can be replaced to some extent to generate new myelin sheaths. This endogenous regeneration capacity has so far mainly been attributed to the activation and recruitment of resident oligodendroglial precursor cells. As this self-repair process is limited and increasingly fails while MS progresses, much interest has evolved regarding the development of remyelination-promoting strateg…

0301 basic medicineCell typeMultiple Sclerosisgliaadult neural stem cellsoligodendrocytesReviewBiologyRegenerative MedicineCatalysisInorganic ChemistryWhite matterlcsh:Chemistry03 medical and health sciencesMyelin0302 clinical medicineNeural Stem CellsmedicineAnimalsHumansPhysical and Theoretical ChemistryRemyelinationMolecular Biologylcsh:QH301-705.5SpectroscopyMyelin SheathMultiple sclerosisRegeneration (biology)Organic ChemistryEndogenous regenerationGeneral Medicinedifferentiationmedicine.diseaseNeural stem cellComputer Science ApplicationsNerve Regeneration030104 developmental biologymedicine.anatomical_structureremyelinationlcsh:Biology (General)lcsh:QD1-999nervous systemprecursor cellsImmunologyNeurosciencecell fate determinationwhite matter030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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Mast cells within cellular networks

2018

Mast cells are highly versatile in terms of their mode of activation by a host of stimuli and their ability to flexibly release a plethora of biologically highly active mediators. Within the immune system, mast cells can best be designated as an active nexus interlinking innate and adaptive immunity. Here we try to draw an arc from initiation of acute inflammatory reactions to microbial pathogens to development of adaptive immunity and allergies. This multifaceted nature of mast cells is made possible by interaction with multiple cell types of immunologic and nonimmunologic origin. Examples for the former include neutrophils, eosinophils, T cells, and professional antigen-presenting cells. …

0301 basic medicineCell typeSensory Receptor CellsNeutrophilsT-LymphocytesImmunologyAntigen-Presenting CellsCell CommunicationAdaptive Immunity03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsHumansImmunology and AllergyMast CellsAntigen-presenting cellToll-like receptorMHC class IIbiologyAcquired immune systemMast cellAsthmaImmunity InnateEosinophilsCrosstalk (biology)030104 developmental biologymedicine.anatomical_structureImmunologybiology.protein030215 immunologyJournal of Allergy and Clinical Immunology
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Spleen tyrosine kinase (SYK) is a potential target for the treatment of cutaneous lupus erythematosus patients

2016

Spleen tyrosine kinase (SYK) is a protein kinase involved in cell proliferation and the regulation of inflammatory pathways. Due to the increasing evidence that kinase inhibitors have potential as specific anti-inflammatory drugs, we have investigated the potential for SYK inhibition as a therapeutic target in autoimmune diseases, particularly cutaneous lupus erythematosus (CLE). Skin samples of patients with different CLE subtypes and appropriate controls were analysed for the expression of SYK and SYK-associated pro-inflammatory mediators via gene expression analysis and immunohistochemistry. The functional role of SYK in keratinocytes was investigated in vitro, using LE-typical pro-infla…

0301 basic medicineCell typeSykchemical and pharmacologic phenomenaDermatologyenvironment and public healthBiochemistry03 medical and health sciencesImmune systemDownregulation and upregulationLupus Erythematosus CutaneousmedicineHumansSyk KinasePhosphorylationMolecular BiologyCells CulturedInnate immune systemSystemic lupus erythematosusKinasebusiness.industryhemic and immune systemsmedicine.diseaseenzymes and coenzymes (carbohydrates)030104 developmental biologyCase-Control StudiesImmunologyCytokinesPhosphorylationbiological phenomena cell phenomena and immunitybusinessExperimental Dermatology
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Trans-presentation of IL-6 by dendritic cells is required for the priming of pathogenic TH17 cells

2016

The cellular sources of interleukin 6 (IL-6) that are relevant for differentiation of the TH17 subset of helper T cells remain unclear. Here we used a novel strategy for the conditional deletion of distinct IL-6-producing cell types to show that dendritic cells (DCs) positive for the signaling regulator Sirpα were essential for the generation of pathogenic TH17 cells. Using their IL-6 receptor α-chain (IL-6Rα), Sirpα+ DCs trans-presented IL-6 to T cells during the process of cognate interaction. While ambient IL-6 was sufficient to suppress the induction of expression of the transcription factor Foxp3 in T cells, trans-presentation of IL-6 by DC-bound IL-6Rα (called 'IL-6 cluster signaling'…

0301 basic medicineCell typebiologyCellular differentiationImmunologyLymphocyte differentiationFOXP3Priming (immunology)medicine.disease_cause3. Good healthCell biologyAutoimmunity03 medical and health sciences030104 developmental biology0302 clinical medicineImmunologybiology.proteinmedicineImmunology and AllergyInterleukin 6Transcription factor030215 immunologyNature Immunology
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