Search results for "auto"

showing 10 items of 10255 documents

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
researchProduct

Autophagy in the pathogenesis of ankylosing spondylitis

2016

The pathogenesis of ankylosing spondylitis (AS) is not well understood, and treatment options have met with limited success. Autophagy is a highly conserved mechanism of controlled digestion of damaged organelles within a cell. It helps in the maintenance of cellular homeostasis. The process of autophagy requires the formation of an isolation membrane. They form double-membraned vesicles called “autophagosomes” that engulf a portion of the cytoplasm. Beyond the role in maintenance of cellular homeostasis, autophagy has been demonstrated as one of the most remarkable tools employed by the host cellular defense against bacteria invasion. Autophagy also affects the immune system and thus is im…

0301 basic medicineCellAutophagy-Related ProteinsATG16L1Cellular homeostasisInflammationBiologyLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Pathogenesis03 medical and health sciencesImmune systemRheumatologyATG16L1; Autophagy; Inflammation; LRRK2; Pathogenesis; Spondyloarthritis; RheumatologyPathogenesiAutophagymedicineHomeostasisHumansSpondylitis AnkylosingATG16L1InflammationAutophagyLRRK2General MedicineCell biology030104 developmental biologymedicine.anatomical_structureCytoplasmSpondyloarthritimedicine.symptomClinical Rheumatology
researchProduct

Tc17 biology and function: Novel concepts

2020

Research over the past years has provided increasing understanding about IL-17-producing CD8+ T cells termed Tc17 or IL-17+ CD8+ T cells, their distribution and role in a range of diverse immune processes. These comprise resistance to pathogens and tissue homeostasis, but also contribution to autoimmunity and cancer, as well as involvement in gut inflammation, lung diseases and graft-versus-host-disease. Tc17 cells are regulated by unique differentiation mechanisms distinguishing them from other IL-17-producing T cells, including Th17, mucosal-associated invariant T cells, and γδ17 T cells, thus ensuring their specific function in immune responses. Here, we review recent advances in underst…

0301 basic medicineCellular differentiationInterleukin-17ImmunologyInflammationCD8-Positive T-LymphocytesBiologymedicine.disease_causeAutoimmunity03 medical and health sciences030104 developmental biology0302 clinical medicineImmune systemT-Lymphocyte SubsetsImmunologymedicineAnimalsHumansImmunology and AllergyCytotoxic T cellInterleukin 17medicine.symptomCD8Tissue homeostasis030215 immunologyEuropean Journal of Immunology
researchProduct

Neurofibromatosis type 2 tumor suppressor protein is expressed in oligodendrocytes and regulates cell proliferation and process formation.

2017

The neurofibromatosis type 2 (NF2) tumor suppressor protein Merlin functions as a negative regulator of cell growth and actin dynamics in different cell types amongst which Schwann cells have been extensively studied. In contrast, the presence and the role of Merlin in oligodendrocytes, the myelin forming cells within the CNS, have not been elucidated. In this work, we demonstrate that Merlin immunoreactivity was broadly distributed in the white matter throughout the central nervous system. Following Merlin expression during development in the cerebellum, Merlin could be detected in the cerebellar white matter tract at early postnatal stages as shown by its co-localization with Olig2-positi…

0301 basic medicineCentral Nervous SystemCytoplasmlcsh:MedicineNervous SystemMyelinMiceCell MovementAnimal CellsCerebellumMedicine and Health SciencesNeurofibromatosis type 2lcsh:ScienceNeuronsStainingCerebral CortexNeurofibromin 2MultidisciplinarybiologyCell StainingBrainCell migrationCell biologyOligodendrogliamedicine.anatomical_structureGenetic DiseasesCell ProcessesAnatomyCellular TypesCellular Structures and OrganellesResearch ArticleCell typeNeurofibromatosis 2NeurogenesisNerve Tissue ProteinsTransfectionResearch and Analysis MethodsCell Line03 medical and health sciencesmedicineAnimalsImmunohistochemistry TechniquesCell ProliferationCell NucleusClinical GeneticsCell growthAutosomal Dominant Diseaseslcsh:RBiology and Life SciencesCell Biologymedicine.diseaseOligodendrocyteMyelin basic proteinMerlin (protein)Mice Inbred C57BLHistochemistry and Cytochemistry Techniques030104 developmental biologySpecimen Preparation and TreatmentAstrocytesNeurofibromatosis Type 2Cellular Neurosciencebiology.proteinImmunologic Techniqueslcsh:QSchwann CellsNeurosciencePLoS ONE
researchProduct

IL-17 controls central nervous system autoimmunity through the intestinal microbiome

2021

Interleukin-17A- (IL-17A) and IL-17F-producing CD4(+) T helper cells (T(H)17 cells) are implicated in the development of chronic inflammatory diseases, such as multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). T-H 17 cells also orchestrate leukocyte invasion of the central nervous system (CNS) and subsequent tissue damage. However, the role of IL-17A and IL-17F as effector cytokines is still confused with the encephalitogenic function of the cells that produce these cytokines, namely, T-H 17 cells, fueling a long-standing debate in the neuroimmunology field. Here, we demonstrated that mice deficient for IL-17A/F lose their susceptibility to EAE, which…

0301 basic medicineCentral Nervous SystemMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisreceptorImmunologyCentral nervous system610 Medicine & healthGut flora10263 Institute of Experimental Immunologymedicine.disease_causeAutoimmunityinterleukin-1703 medical and health sciencesMice0302 clinical medicinemedicinecytokineAnimalsHumanscnst-cellsMice Knockout2403 Immunologybiologygut microbiotaMultiple sclerosisExperimental autoimmune encephalomyelitisGeneral MedicineFecal Microbiota Transplantationneutralizationmedicine.diseasebiology.organism_classificationAdoptive Transfer3. Good healthGut EpitheliumGastrointestinal Microbiome030104 developmental biologyNeuroimmunologymedicine.anatomical_structureImmunology2723 Immunology and Allergy570 Life sciences; biologyTh17 CellssequencesFemaleInterleukin 17030217 neurology & neurosurgery
researchProduct

Bifidobacterium CECT 7765 modulates early stress-induced immune, neuroendocrine and behavioral alterations in mice.

2016

Emerging evidence suggests that there is a window of opportunity within the early developmental period, when microbiota-based interventions could play a major role in modulating the gut-brain axis and, thereby, in preventing mood disorders. This study aims at evaluating the effects and mode of action of Bifidobacterium pseudocatenulatum CECT 7765 in a murine model of chronic stress induced by maternal separation (MS). C57Bl/6J male breast-fed pups were divided into four groups, which were subjected or not to MS and supplemented with placebo or B. pseudocatenulatum CECT7765 until postnatal period (P) 21 and followed-up until P41. Behavioral tests were performed and neuroendocrine parameters …

0301 basic medicineCentral Nervous SystemMalemedicine.medical_specialtyHypothalamo-Hypophyseal Systemmedicine.medical_treatmentImmunologyBifidobacterium pseudocatenulatumPituitary-Adrenal SystemInflammationBiologyDiet High-Fat03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compoundMice0302 clinical medicineImmune systemCorticosteroneStress PhysiologicalInternal medicineRNA Ribosomal 16SmedicineAnimalsChronic stressObesityNeurotransmitterInflammationNeurotransmitter AgentsEndocrine and Autonomic SystemsMaternal DeprivationMicrobiotaProbioticsNeurosecretory SystemsIntestinesMice Inbred C57BL030104 developmental biologyCytokineEndocrinologychemistryHypothalamusImmunologyDietary SupplementsCytokinesBifidobacteriummedicine.symptom030217 neurology & neurosurgeryBrain, behavior, and immunity
researchProduct

CNS-localized myeloid cells capture living invading T cells during neuroinflammation

2020

Using an in vivo real-time approach, the authors show that local myeloid cells remove early CNS-invading T cells via an engulfment pathway that is dependent on N-acetyl-D-glucosamine (GlcNAc) and lectin. These results reveal a novel capacity of myeloid cells to counteract neuroinflammation.

0301 basic medicineCentral Nervous SystemProgrammed cell deathCell signalingEncephalomyelitis Autoimmune ExperimentalCell SurvivalEncephalomyelitisT cellT-LymphocytesImmunologyInnate Immunity and InflammationCX3C Chemokine Receptor 1AutoimmunityReceptors Cell SurfaceCell CommunicationPhosphatidylserinesBiologyLymphocyte ActivationSeverity of Illness IndexArticle03 medical and health sciencesMice0302 clinical medicineNeuroinflammationPhagocytosisIn vivomedicineImmunology and AllergyAnimalsLectins C-TypeMyeloid CellsNeuroinflammationInflammationGlucosamineCell DeathExperimental autoimmune encephalomyelitismedicine.diseaseCell biology030104 developmental biologymedicine.anatomical_structureMannose-Binding LectinsTh17 Cells030217 neurology & neurosurgeryEx vivoMannose ReceptorThe Journal of Experimental Medicine
researchProduct

Targeting Voltage-Dependent Calcium Channels with Pregabalin Exerts a Direct Neuroprotective Effect in an Animal Model of Multiple Sclerosis

2018

Background/aims Multiple sclerosis (MS) is a prototypical autoimmune central nervous system (CNS) disease. Particularly progressive forms of MS (PMS) show significant neuroaxonal damage as consequence of demyelination and neuronal hyperexcitation. Immuno-modulatory treatment strategies are beneficial in relapsing MS (RMS), but mostly fail in PMS. Pregabalin (Lyrica®) is prescribed to MS patients to treat neuropathic pain. Mechanistically, it targets voltage-dependent Ca2+ channels and reduces harmful neuronal hyperexcitation in mouse epilepsy models. Studies suggest that GABA analogues like pregabalin exert neuroprotective effects in animal models of ischemia and trauma. Methods We tested t…

0301 basic medicineCentral nervous systemPregabalinPregabalinPharmacologyNeuroprotectionlcsh:RC346-429Multiple sclerosis03 medical and health sciencesCellular and Molecular NeuroscienceDevelopmental Neurosciencemedicinelcsh:Neurology. Diseases of the nervous systemExperimental autoimmune encephalomyelitisMicrogliaVoltage-dependent calcium channelbusiness.industryMultiple sclerosislcsh:QP351-495Experimental autoimmune encephalomyelitismedicine.diseaseNeuroprotectionlcsh:Neurophysiology and neuropsychology030104 developmental biologymedicine.anatomical_structureNeurologyNeuropathic painbusinessmedicine.drugNeurosignals
researchProduct

IL-10-Modulated Human Dendritic Cells for Clinical Use: Identification of a Stable and Migratory Subset with Improved Tolerogenic Activity.

2015

Abstract Dendritic cells (DCs) are key regulators of protective immune responses and tolerance to (self-)Ags. Therefore, the scientific rationale for the use of tolerogenic DC therapy in the fields of allergies, autoimmunity, and transplantation medicine is strong. In this study, we analyzed the tolerogenic capacity of IL-10–modulated DC (IL-10DC) subpopulations to identify a DC subset that combines potent immunosuppressive activities with valuable immune properties for clinical implementation. IL-10DCs consist of two phenotypically distinct subpopulations: CD83highCCR7+ IL-10DCs and CD83lowCCR7− IL-10DCs. Suppressor assays with activated effector T cells revealed that CD4+ regulatory T cel…

0301 basic medicineChemokineReceptors CCR7medicine.medical_treatmentImmunologyImmunoglobulinsBiologymedicine.disease_causeLymphocyte ActivationT-Lymphocytes RegulatoryAutoimmunity03 medical and health sciencesImmune systemAntigens CDCell MovementmedicineImmune ToleranceImmunology and AllergyHumansIL-2 receptorCells CulturedInflammationMembrane GlycoproteinsChemokine CCL21Interleukin-2 Receptor alpha SubunitCell DifferentiationDendritic CellsInterleukin-10Interleukin 10Tolerance induction030104 developmental biologyCytokineImmunologybiology.proteinImmunotherapyCCL21Journal of immunology (Baltimore, Md. : 1950)
researchProduct

Single-cell profiling reveals GPCR heterogeneity and functional patterning during neuroinflammation.

2017

GPCR expression was intensively studied in bulk cDNA of leukocyte populations, but limited data are available with respect to expression in individual cells. Here, we show a microfluidic-based single-cell GPCR expression analysis in primary T cells, myeloid cells, and endothelial cells under naive conditions and during experimental autoimmune encephalomyelitis, the mouse model of multiple sclerosis. We found that neuroinflammation induces characteristic changes in GPCR heterogeneity and patterning, and we identify various functionally relevant subgroups with specific GPCR profiles among spinal cord-infiltrating CD4 T cells, macrophages, microglia, or endothelial cells. Using GPCRs CXCR4, S1…

0301 basic medicineChemokinebiologyMicrogliaExperimental autoimmune encephalomyelitisCellInflammationGeneral Medicinemedicine.diseaseCell biology03 medical and health sciences030104 developmental biologymedicine.anatomical_structureImmune systemmedicinebiology.proteinmedicine.symptomNeuroinflammationG protein-coupled receptorResearch ArticleJCI insight
researchProduct