Search results for " Autoimmune"

showing 10 items of 252 documents

Graph Theoretical Framework of Brain Networks in Multiple Sclerosis: A Review of Concepts.

2019

Abstract Network science provides powerful access to essential organizational principles of the human brain. It has been applied in combination with graph theory to characterize brain connectivity patterns. In multiple sclerosis (MS), analysis of the brain networks derived from either structural or functional imaging provides new insights into pathological processes within the gray and white matter. Beyond focal lesions and diffuse tissue damage, network connectivity patterns could be important for closely tracking and predicting the disease course. In this review, we describe concepts of graph theory, highlight novel issues of tissue reorganization in acute and chronic neuroinflammation an…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisModels NeurologicalNetwork science03 medical and health sciences0302 clinical medicineNeural PathwaysmedicineAnimalsHumansGeneral NeuroscienceMultiple sclerosisBrainGraph theoryHuman brainmedicine.diseaseFunctional imaging030104 developmental biologymedicine.anatomical_structureGraph (abstract data type)DisconnectionPsychologyNeuroscience030217 neurology & neurosurgeryNetwork analysisNeuroscience
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Gatekeeper role of brain antigen‐presenting CD11c + cells in neuroinflammation

2015

Multiple sclerosis is the most frequent chronic inflammatory disease of the CNS. The entry and survival of pathogenic T cells in the CNS are crucial for the initiation and persistence of autoimmune neuroinflammation. In this respect, contradictory evidence exists on the role of the most potent type of antigen-presenting cells, dendritic cells. Applying intravital two-photon microscopy, we demonstrate the gatekeeper function of CNS professional antigen-presenting CD11c(+) cells, which preferentially interact with Th17 cells. IL-17 expression correlates with expression of GM-CSF by T cells and with accumulation of CNS CD11c(+) cells. These CD11c(+) cells are organized in perivascular clusters…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT-LymphocytesAntigen-Presenting CellsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesInterleukin 210302 clinical medicineCell MovementAnimalsCytotoxic T cellAntigen-presenting cellMolecular BiologyNeuroinflammationInterleukin 3CD40General Immunology and MicrobiologybiologyGeneral NeuroscienceInterleukin-17BrainGranulocyte-Macrophage Colony-Stimulating Factorhemic and immune systemsDendritic CellsArticlesNatural killer T cellCD11c AntigenMice Inbred C57BL030104 developmental biologyImmunologyInterleukin 12biology.proteinTh17 Cells030215 immunologyThe EMBO Journal
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TGF-β inhibitor Smad7 regulates dendritic cell-induced autoimmunity

2017

TGF-β is an anti-inflammatory cytokine whose signaling is negatively controlled by Smad7. Previously, we established a role for Smad7 in the generation of autoreactive T cells; however, the function of Smad7 in dendritic cells (DCs) remains elusive. Here, we demonstrate that DC-specific Smad7 deficiency resulted in elevated expression of the transcription factors Batf3 and IRF8, leading to increased frequencies of CD8(+)CD103(+) DCs in the spleen. Furthermore, Smad7-deficient DCs expressed higher levels of indoleamine 2,3-dioxygenase (IDO), an enzyme associated with tolerance induction. Mice devoid of Smad7 specifically in DCs are resistant to the development of experimental autoimmune ence…

0301 basic medicineEncephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentCellular differentiationAutoimmunitychemical and pharmacologic phenomenaCD8-Positive T-LymphocytesBiologyT-Lymphocytes RegulatorySmad7 ProteinImmune toleranceMice03 medical and health sciences0302 clinical medicineTransforming Growth Factor betaImmune TolerancemedicineAnimalsIndoleamine-Pyrrole 23-DioxygenaseMultidisciplinaryintegumentary systemExperimental autoimmune encephalomyelitisCell Differentiationhemic and immune systemsDendritic CellsDendritic cellTransforming growth factor betamedicine.diseaseCell biologyMice Inbred C57BLTolerance inductionBasic-Leucine Zipper Transcription Factors030104 developmental biologyCytokinePNAS PlusInterferon Regulatory FactorsImmunologybiology.proteinCytokinesSpleenCD8Signal Transduction030215 immunology
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Role of the epigenetic factor Sirt7 in neuroinflammation and neurogenesis.

2017

Epigenetic regulators are increasingly recognized as relevant modulators in the immune and nervous system. The class of sirtuins consists of NAD+-dependent histone deacetylases that regulate transcription. Sirtuin family member Sirt1 has already been shown to influence the disease course in an animal model of autoimmune neuroinflammation (experimental autoimmune encephalomyelitis (EAE). A role of Sirt7, a related epigenetic regulator, on immune system regulation has been proposed before, as these mice are more susceptible to develop inflammatory cardiomyopathy. Sirt7-/- animals showed no differences in clinical score compared to wild-type littermates after EAE induction with myelin oligoden…

0301 basic medicineEpigenetic regulation of neurogenesisEncephalomyelitis Autoimmune ExperimentalNeurogenesisAdaptive ImmunityHippocampusT-Lymphocytes RegulatoryMyelin oligodendrocyte glycoproteinEpigenesis Genetic03 medical and health sciencesImmune systemmedicineAnimalsSirtuinsNeuroinflammationCell ProliferationMice KnockoutNeuronsbiologyGeneral NeuroscienceExperimental autoimmune encephalomyelitisNeurogenesisGeneral Medicinemedicine.diseaseAcquired immune systemMice Inbred C57BL030104 developmental biologyImmunologySirtuinbiology.proteinEncephalitisFemaleNeuroscienceNeuroscience research
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Guidelines for biomarkers in autoimmune rheumatic diseases - evidence based analysis

2018

Autoimmune rheumatic diseases are characterised by an abnormal immune system response, complement activation, cytokines dysregulation and inflammation. In last years, despite many progresses in managing these patients, it has been shown that clinical remission is reached in less than 50% of patients and a personalised and tailored therapeutic approach is still lacking resulting in a significant gap between guidelines and real-world practice. In this context, the need for biomarkers facilitating early diagnosis and profiling those individuals at the highest risk for a poor outcome has become of crucial interest. A biomarker generally refers to a measured characteristic which may be used as a…

0301 basic medicineEvidence-based practiceImmunologyInflammationGuidelines as TopicSystemic lupus erythematosuBioinformaticsAntiphospholipid syndrome; Biomarker; Rheumatoid arthritis; Sjögren syndrome; Spondyloarthritides; Systemic lupus erythematosus; Systemic sclerosis;Autoimmune DiseaseAutoimmune DiseasesRheumatic Disease03 medical and health sciencesTherapeutic approachSystemic sclerosiEconomica0302 clinical medicineImmune systemSystemic lupus erythematosusAntiphospholipid syndromeEarly DiagnosiRheumatic DiseasesAntiphospholipid syndromemedicineImmunology and AllergyHumansRheumatoid arthritisRheumatoid arthritiAntiphospholipid syndrome; Biomarker; Rheumatoid arthritis; Sjögren syndrome; Spondyloarthritides; Systemic lupus erythematosus; Systemic sclerosis030203 arthritis & rheumatologySpondyloarthritidebusiness.industryBiomarkermedicine.diseaseClinical diseaseSjögren syndromeAntiphospholipid syndrome; Biomarker; Rheumatoid arthritis; Sjögren syndrome; Spondyloarthritides; Systemic lupus erythematosus; Systemic sclerosis; Autoimmune Diseases; Biomarkers; Early Diagnosis; Evidence-Based Practice; Guidelines as Topic; Humans; Rheumatic Diseases; Immunology and Allergy; ImmunologySettore MED/16 - Reumatologia030104 developmental biologyEarly DiagnosisRheumatoid arthritisEvidence-Based PracticeBiomarker (medicine)SpondyloarthritidesSystemic sclerosismedicine.symptombusinessBiomarkersHuman
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The Role of ERK Signaling in Experimental Autoimmune Encephalomyelitis

2017

Extracellular signal-regulated kinase (ERK) signaling plays a crucial role in regulating immune cell function and has been implicated in autoimmune disorders. To date, all commercially available inhibitors of ERK target upstream components, such as mitogen-activated protein (MAP) kinase/ERK kinase (MEKs), but not ERK itself. Here, we directly inhibit nuclear ERK translocation by a novel pharmacological approach (Glu-Pro-Glu (EPE) peptide), leading to an increase in cytosolic ERK phosphorylation during T helper (Th)17 cell differentiation. This was accompanied by diminished secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine influencing the encephalitogenicity …

0301 basic medicineMAPK/ERK pathwaymedicine.medical_treatmentCellular differentiationexperimental autoimmune encephalomyelitisLymphocyte Activationmedicine.disease_causemultiple sclerosisAutoimmunitylcsh:ChemistryMice0302 clinical medicineT-Lymphocyte SubsetsPhosphorylationExtracellular Signal-Regulated MAP Kinaseslcsh:QH301-705.5SpectroscopyKinaseExperimental autoimmune encephalomyelitisInterleukinGeneral MedicineComputer Science ApplicationsCell biologyProtein TransportCytokine030220 oncology & carcinogenesisFemaleERK pathwayCell signalingEncephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemT cellsBiologyModels BiologicalArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalscell signalingPhysical and Theoretical ChemistryEPE peptideMolecular BiologyT cells; ERK pathway; EPE peptide; experimental autoimmune encephalomyelitis; multiple sclerosis; cell signalingOrganic ChemistryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Th17 CellsInternational Journal of Molecular Sciences
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Initial serum thyroid peroxidase antibodies and long-term outcomes in SREAT.

2015

Objective To quantify clinical outcome in patients with steroid-responsive encephalopathy and associated autoimmune thyroiditis (SREAT) after the acute phase and explore potential associations of initial serum thyroid peroxidase antibody titers (TPO-Abs) with outcome. Materials and methods Retrospective chart review of patients diagnosed with SREAT between 01/2005 and 05/2014 in a tertiary care center and followed in an affiliated autoimmune outpatient clinic. Outcome was quantified using the extended Glasgow Outcome Scale (GOS-E). We calculated Pearson's correlation coefficients to quantify associations with clinical outcome at follow-up. Results Among 134 patients with encephalopathy of u…

0301 basic medicineMaleAnti-Inflammatory AgentsGlasgow Outcome Scaleblood [Iodide Peroxidase]0302 clinical medicineblood [Hashimoto Disease]blood [Encephalitis]Outpatient clinicHashimoto Diseasebiologytherapy [Hashimoto Disease]Glasgow Outcome Scaletherapy [Encephalitis]therapeutic use [Anti-Inflammatory Agents]General MedicineMiddle Agedblood [Thyroiditis Autoimmune]Magnetic Resonance Imagingtherapy [Thyroiditis Autoimmune]Treatment OutcomeNeurologyEncephalitisFemaleSteroidsImmunosuppressive AgentsAdultmedicine.medical_specialtyEncephalopathyHashimoto DiseaseIodide PeroxidaseAutoimmune thyroiditisanalysis [Autoantibodies]03 medical and health sciencesimmunology [Thyroiditis Autoimmune]Thyroid peroxidaseInternal medicinemedicineHumansddc:610immunology [Encephalitis]therapeutic use [Steroids]AgedAutoantibodiesRetrospective Studiesbusiness.industrytherapeutic use [Methotrexate]Thyroiditis AutoimmuneRetrospective cohort studymedicine.diseasetherapeutic use [Immunosuppressive Agents]immunology [Hashimoto Disease]030104 developmental biologyMethotrexateImmunologybiology.proteinEtiologyNeurology (clinical)businessimmunology [Iodide Peroxidase]030217 neurology & neurosurgeryFollow-Up StudiesActa neurologica Scandinavica
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General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation.

2016

Relapsing-remitting multiple sclerosis (MS)(2) is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).(3) The molecular mechanisms responsible for directing Tregs into the inflamed CNS tissue, however, are incompletely understood. In an MS mouse model we show that the stress kinase general control non-derepressible 2 (GCN2),(4) expressed in T cells, contributes to the resolution of autoimmune neuroinflammation. Failure to recover from acute inflammation was associated with reduced frequencies of CNS-infiltrating Tregs. GCN2 deficient Tregs displayed impaired migration to a…

0301 basic medicineMaleChemokineEncephalomyelitis Autoimmune ExperimentalTime FactorsT cellImmunologyInflammationSpontaneous remissionMice TransgenicCCL2Protein Serine-Threonine KinasesT-Lymphocytes RegulatoryStatistics Nonparametric03 medical and health sciencesMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsAnnexin A5NeuroinflammationbiologyKinaseMultiple sclerosisBrainEndothelial Cellsmedicine.diseaseFlow CytometryPeptide FragmentsMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesImmunologybiology.proteinDisease ProgressionCytokinesFemaleMyelin-Oligodendrocyte GlycoproteinNeurology (clinical)medicine.symptom030215 immunologyJournal of neuroimmunology
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Blimp1 Prevents Methylation of Foxp3 and Loss of Regulatory T Cell Identity at Sites of Inflammation

2018

Summary Foxp3+ regulatory T (Treg) cells restrict immune pathology in inflamed tissues; however, an inflammatory environment presents a threat to Treg cell identity and function. Here, we establish a transcriptional signature of central nervous system (CNS) Treg cells that accumulate during experimental autoimmune encephalitis (EAE) and identify a pathway that maintains Treg cell function and identity during severe inflammation. This pathway is dependent on the transcriptional regulator Blimp1, which prevents downregulation of Foxp3 expression and “toxic” gain-of-function of Treg cells in the inflamed CNS. Blimp1 negatively regulates IL-6- and STAT3-dependent Dnmt3a expression and function …

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalBlimp1CNS2Regulatory T cellInflammationchemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyArticleepigenetic regulationDNA Methyltransferase 3AEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineImmune systemDownregulation and upregulationmedicineAnimalsEpigeneticsDNA (Cytosine-5-)-Methyltransferaseslcsh:QH301-705.5Regulation of gene expressionInterleukin-6FOXP3Forkhead Transcription FactorsDNA methyltransferaseshemic and immune systemsDNA Methylation3. Good healthCell biologyddc:Mice Inbred C57BL030104 developmental biologymedicine.anatomical_structureregulatory T cellslcsh:Biology (General)inflammationFoxp3DNA methylationFemalePositive Regulatory Domain I-Binding Factor 1medicine.symptomCNS030217 neurology & neurosurgeryCell Reports
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Fast direct neuronal signaling via the IL-4 receptor as therapeutic target in neuroinflammation.

2018

Ongoing axonal degeneration is thought to underlie disability in chronic neuroinflammation, such as multiple sclerosis (MS), especially during its progressive phase. Upon inflammatory attack, axons undergo pathological swelling, which can be reversible. Because we had evidence for beneficial effects of T helper 2 lymphocytes in experimental neurotrauma and discovered interleukin-4 receptor (IL-4R) expressed on axons in MS lesions, we aimed at unraveling the effects of IL-4 on neuroinflammatory axon injury. We demonstrate that intrathecal IL-4 treatment during the chronic phase of several experimental autoimmune encephalomyelitis models reversed disease progression without affecting inflamma…

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisEncephalomyelitisInflammation03 medical and health sciencesMice0302 clinical medicinemedicineAnimalsHumansAxonReceptorNeuroinflammationAdministration IntranasalInflammationNeuronsbusiness.industryMultiple sclerosisExperimental autoimmune encephalomyelitisTranslation (biology)General Medicinemedicine.diseaseAxonsReceptors Interleukin-4030104 developmental biologymedicine.anatomical_structurenervous systemInterleukin-4medicine.symptombusinessNeuroscience030217 neurology & neurosurgeryLocomotionScience translational medicine
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