Search results for "autoimmune"

showing 10 items of 648 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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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
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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
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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
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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
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Towards patient stratification and treatment in the autoimmune disease lupus erythematosus using a systems pharmacology approach

2015

Drug development in Systemic Lupus Erythematosus (SLE) has been hindered by poor translation from successful preclinical experiments to clinical efficacy. This lack of success has been attributed to the high heterogeneity of SLE patients and to the lack of understanding of disease physiopathology. Modelling approaches could be useful for supporting the identification of targets, biomarkers and patient subpopulations with differential response to drugs. However, the use of traditional quantitative models based on differential equations is not justifiable in a sparse data situation. Boolean networks models are less demanding on the required data to be implemented and can provide insights into…

0301 basic medicineDrugSystems biologymedia_common.quotation_subjectPharmaceutical ScienceAntineoplastic AgentsDiseaseBioinformaticsAutoimmune Diseases03 medical and health sciencesmedicineAnimalsCluster AnalysisHumansLupus Erythematosus SystemicComputer Simulationmedia_commonAutoimmune diseaseLupus erythematosusbusiness.industrySystems Biologymedicine.diseaseTreatment Outcome030104 developmental biologyDrug developmentPharmacology ClinicalbusinessBiological networkSystems pharmacologyEuropean Journal of Pharmaceutical Sciences
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The more the merrier? Scoring, statistics and animal welfare in experimental autoimmune encephalomyelitis.

2016

Experimental autoimmune encephalomyelitis (EAE) is a frequently used animal model for the investigation of autoimmune processes in the central nervous system. As such, EAE is useful for modelling certain aspects of multiple sclerosis, a human autoimmune disease that leads to demyelination and axonal destruction. It is an important tool for investigating pathobiology, identifying drug targets and testing drug candidates. Even though EAE is routinely used in many laboratories and is often part of the routine assessment of knockouts and transgenes, scoring of the disease course has not become standardized in the community, with at least 83 published scoring variants. Varying scales with diffe…

0301 basic medicineEncephalomyelitis Autoimmune Experimental3400 General Veterinary610 Medicine & healthAnimal WelfareDisease course03 medical and health sciences0302 clinical medicineAnimal modelAnimals LaboratorymedicineAnimalsStatistical analysis10239 Institute of Laboratory Animal SciencerefinementAutoimmune diseasescoring scalesGeneral VeterinaryAnimal Welfare (journal)business.industryEAEMultiple sclerosisExperimental autoimmune encephalomyelitismedicine.diseasehumane endpointsDisease Models Animal030104 developmental biologyResearch DesignAnimals Domestic570 Life sciences; biologyAnimal Science and Zoology1103 Animal Science and ZoologybusinessNeuroscience030217 neurology & neurosurgeryLaboratory animals
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IL ‐1 signaling is critical for expansion but not generation of autoreactive GM ‐ CSF + Th17 cells

2016

Abstract Interleukin‐1 (IL‐1) is implicated in numerous pathologies, including multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the exact mechanism by which IL‐1 is involved in the generation of pathogenic T cells and in disease development remains largely unknown. We found that following EAE induction, pertussis toxin administration leads to IL‐1 receptor type 1 (IL‐1R1)‐dependent IL‐1β expression by myeloid cells in the draining lymph nodes. This myeloid‐derived IL‐1β did not vitally contribute to the generation and plasticity of Th17 cells, but rather promoted the expansion of a GM‐CSF + Th17 cell subset, thereby enhancing its encephalitog…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalBiologymedicine.disease_causePertussis toxinGeneral Biochemistry Genetics and Molecular BiologyAutoimmunityMice03 medical and health sciences0302 clinical medicineMediatormedicineAnimalsInducerMolecular BiologyCell ProliferationGeneral Immunology and MicrobiologyGeneral NeuroscienceMultiple sclerosisExperimental autoimmune encephalomyelitisGranulocyte-Macrophage Colony-Stimulating FactorArticlesmedicine.diseaseCell biology030104 developmental biologyPertussis ToxinT cell subsetImmunologyTh17 CellsLymphInterleukin-1030215 immunologyThe EMBO Journal
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Targeting CD52 does not affect murine neuron and microglia function.

2020

The humanized anti-CD52 antibody alemtuzumab is successfully used in the treatment of multiple sclerosis (MS) and is thought to exert most of its therapeutic action by depletion and repopulation of mainly B and T lymphocytes. Although neuroprotective effects of alemtuzumab have been suggested, direct effects of anti-CD52 treatment on glial cells and neurons within the CNS itself have not been investigated so far. Here, we show CD52 expression in murine neurons, astrocytes and microglia, both in vitro and in vivo. As expected, anti CD52-treatment caused profound lymphopenia and improved disease symptoms in mice subjected to experimental autoimmune encephalomyelitis (EAE). CD52 blockade also …

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalCD52Excitotoxicitymedicine.disease_causeNeuroprotection03 medical and health sciencesMice0302 clinical medicinemedicineAnimalsAlemtuzumabPharmacologyNeuronsMicrogliabusiness.industryMultiple sclerosisExperimental autoimmune encephalomyelitismedicine.disease030104 developmental biologymedicine.anatomical_structureCD52 AntigenGene Expression RegulationAlemtuzumabCalciumNeuronMicrogliabusinessNeuroscience030217 neurology & neurosurgerymedicine.drugEuropean journal of pharmacology
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Dendritic cells tip the balance towards induction of regulatory T cells upon priming in experimental autoimmune encephalomyelitis

2016

Counter-balancing regulatory mechanisms, such as the induction of regulatory T cells (Treg), limit the effects of autoimmune attack in neuroinflammation. However, the role of dendritic cells (DCs) as the most powerful antigen-presenting cells, which are intriguing therapeutic targets in this context, is not fully understood. Here, we demonstrate that conditional ablation of DCs during the priming phase of myelin-specific T cells in experimental autoimmune encephalomyelitis (EAE) selectively aborts inducible Treg (iTreg) induction, whereas generation of T helper (Th)1/17 cells is unaltered. DCs facilitate iTreg induction by creating a milieu with high levels of interleukin (IL)-2 due to a st…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalImmunologyMedizinPriming (immunology)chemical and pharmacologic phenomenaAutoimmunitymedicine.disease_causeLymphocyte ActivationT-Lymphocytes RegulatoryAutoimmunityImmunomodulation03 medical and health sciencesMice0302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betamedicineImmunology and AllergyAnimalsNeuroinflammationCD40biologyMultiple sclerosisExperimental autoimmune encephalomyelitisInterleukinhemic and immune systemsDendritic Cellsmedicine.disease030104 developmental biologyImmunologybiology.proteinInterleukin 12CytokinesTh17 Cells030217 neurology & neurosurgery
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