Search results for "Elitis"

showing 10 items of 226 documents

Fighting mycobacterial infections by antibiotics, phytochemicals and vaccines.

2011

Buruli ulcer is a neglected disease caused by Mycobacterium ulcerans and represents the world's third most common mycobacterial infection. It produces the polyketide toxins, mycolactones A, B, C and D, which induce apoptosis and necrosis. Clinical symptoms are subcutaneous nodules, papules, plaques and ulcerating oedemae, which can enlarge and destroy nerves and blood vessels and even invade bones by lymphatic or haematogenous spread (osteomyelitis). Patients usually do not suffer from pain or systematic inflammation. Surgery is the treatment of choice, although recurrence is common and wide surgical excisions including healthy tissues result in significant morbidity. Antibiotic therapy wit…

Buruli ulcerNecrosismedicine.drug_classImmunologyAntibioticsBacterial ToxinsInflammationApoptosisQuinolonesMicrobiologyNecrosisBacterial ProteinsmedicineVaccines DNAAnimalsHumansBuruli UlcerbiologyMycobacterium ulceransbusiness.industryOsteomyelitisVaccinationNeglected DiseasesChaperonin 60medicine.diseasebiology.organism_classificationRifamycinsAnti-Bacterial AgentsVaccinationInfectious DiseasesLymphatic systemAminoglycosidesMycobacterium ulceransImmunologyBacterial VaccinesMacrolidesmedicine.symptombusinessPhytotherapyMicrobes and infection
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Chemokine receptor CCR7 on CD4+ T cells plays a crucial role in the induction of experimental autoimmune encephalomyelitis

2014

CCR1Chemokine receptorNeurologyImmunologyExperimental autoimmune encephalomyelitisImmunologymedicineImmunology and AllergyC-C chemokine receptor type 7Neurology (clinical)Biologymedicine.diseaseCXCR3Journal of Neuroimmunology
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The Cytokine GM-CSF Drives the Inflammatory Signature of CCR2+ Monocytes and Licenses Autoimmunity.

2015

Granulocyte-macrophage colony-stimulating factor (GM-CSF) has emerged as a crucial cytokine produced by auto-reactive T helper (Th) cells that initiate tissue inflammation. Multiple cell types can sense GM-CSF, but the identity of the pathogenic GM-CSF-responsive cells is unclear. By using conditional gene targeting, we systematically deleted the GM-CSF receptor (Csf2rb) in specific subpopulations throughout the myeloid lineages. Experimental autoimmune encephalomyelitis (EAE) progressed normally when either classical dendritic cells (cDCs) or neutrophils lacked GM-CSF responsiveness. The development of tissue-invading monocyte-derived dendritic cells (moDCs) was also unperturbed upon Csf2r…

CCR2Myeloidmedicine.medical_treatmentInterleukin-1betaAutoimmunitymedicine.disease_causeMonocytesAutoimmunityCytokine Receptor Common beta Subunit0302 clinical medicineSTAT5 Transcription FactorImmunology and AllergyAntigens LyMyeloid CellsPhosphorylationMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionExperimental autoimmune encephalomyelitisGene targetingFlow CytometryInfectious DiseasesCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factor2723 Immunology and Allergymedicine.symptommedicine.drugSignal TransductionEncephalomyelitis Autoimmune ExperimentalReceptors CCR2Immunology610 Medicine & healthInflammationMice TransgenicBiology03 medical and health sciencesmedicineAnimalsHumans030304 developmental biologyInflammation2403 ImmunologyGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesDendritic Cellsmedicine.disease10040 Clinic for NeurologyImmunologyTranscriptome030217 neurology & neurosurgery
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The role of CD8+ T cells and their local interaction with CD4+ T cells in myelin oligodendrocyte glycoprotein35-55-induced experimental autoimmune en…

2013

Abstract T cells have an essential role in the induction of multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). Although for CD4+ T cells it is well established that they contribute to the disease, less is known about the role of CD8+ T cells. Our aim was to determine the individual contribution of CD4+ and CD8+ T cells in myelin oligodendrocyte glycoprotein (MOG)35–55–induced EAE. We investigated MOG35–55–activated CD8+ T cells to clarify their potential to induce or attenuate EAE. We monitored the behavior of CD8+ T cells and their interaction with CD4+ T cells directly at the site of inflammation in the CNS using intravital imaging of the brainstem of…

CD4-Positive T-LymphocytesCentral Nervous SystemEncephalomyelitis Autoimmune ExperimentalT cellImmunologyMedizinCell CommunicationCD8-Positive T-LymphocytesLymphocyte ActivationInterleukin 21MiceCell MovementmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorInflammationMice KnockoutCD40biologyCD28Molecular biologyPeptide FragmentsMice Inbred C57BLmedicine.anatomical_structureImmunologybiology.proteinInterleukin 12Myelin-Oligodendrocyte GlycoproteinCD8Journal of immunology (Baltimore, Md. : 1950)
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Cross-recognition of a myelin peptide by CD8+ T cells in the CNS is not sufficient to promote neuronal damage.

2015

Multiple sclerosis (MS) is an inflammatory disease of the CNS thought to be driven by CNS-specific T lymphocytes. Although CD8+T cells are frequently found in multiple sclerosis lesions, their distinct role remains controversial because direct signs of cytotoxicity have not been confirmedin vivo. In the present work, we determined that murine ovalbumin-transgenic (OT-1) CD8+T cells recognize the myelin peptide myelin oligodendrocyte glycoprotein 40–54 (MOG40–54) bothin vitroandin vivo. The aim of this study was to investigate whether such cross-recognizing CD8+T cells are capable of inducing CNS damagein vivo. Using intravital two-photon microscopy in the mouse model of multiple sclerosis, …

CD4-Positive T-LymphocytesCentral Nervous SystemMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisAutoimmunityMice TransgenicCD8-Positive T-Lymphocytesmedicine.disease_causeMyelin oligodendrocyte glycoproteinMyelinMiceIn vivomedicineCytotoxic T cellAnimalsCells CulturedCell ProliferationbiologyCell DeathGeneral NeuroscienceMultiple sclerosisArticlesmedicine.diseaseMolecular mimicrymedicine.anatomical_structureImmunologyNerve Degenerationbiology.proteinFemaleMyelin-Oligodendrocyte GlycoproteinCD8Intravital microscopyThe Journal of neuroscience : the official journal of the Society for Neuroscience
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Modulation of dendritic cell properties by laquinimod as a mechanism for modulating multiple sclerosis.

2013

Laquinimod is an orally administered compound that is under investigation in relapsing-remitting multiple sclerosis. To understand the mechanism by which laquinimod exerts its clinical effects, we have performed human and murine studies assessing its immunomodulatory properties. In experimental autoimmune encephalomyelitis, the therapeutic administration of laquinimod beginning during the recovery of SJL mice, prevented further relapses as expected and strongly reduced infiltration of CD4+ and CD8+ T cells in the central nervous system. We hypothesized that this beneficial effect was mediated by dendritic cells, since we and others found a modulation of different dendritic cell subsets unde…

CD4-Positive T-LymphocytesChemokineEncephalomyelitis Autoimmune ExperimentalT cellQuinoloneschemistry.chemical_compoundMiceMultiple Sclerosis Relapsing-RemittingmedicineAnimalsHumansbiologyMonocyteExperimental autoimmune encephalomyelitisNF-kappa BDendritic cellDendritic Cellsmedicine.diseaseMice Inbred C57BLmedicine.anatomical_structurechemistryImmunologybiology.proteinCytokine secretionFemaleNeurology (clinical)LaquinimodCD8Brain : a journal of neurology
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New candidates for CD4 T cell pathogenicity in experimental neuroinflammation and multiple sclerosis

2015

Multiple sclerosis is a chronic autoimmune demyelinating disease of the central nervous system, which is thought to be triggered by environmental factors in genetically susceptible individuals leading to activation of autoreactive T lymphocytes. Large multi-centre genome-wide association studies have identified multiple genetic risk loci in multiple sclerosis. In this study, we investigated T cell transcriptomic changes in experimental autoimmune encephalomyelitis, an animal model for multiple sclerosis. We correlated these findings with the multiple sclerosis risk genes postulated by the most recent Immunochip analysis and found that multiple sclerosis susceptibility genes were significant…

CD4-Positive T-LymphocytesMice KnockoutEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisEffectorMultiple sclerosisT cellExperimental autoimmune encephalomyelitisGenome-wide association studyMERTKBiologymedicine.diseaseMice Inbred C57BLMicemedicine.anatomical_structureImmunologymedicineDemyelinating diseaseAnimalsHumansGene Regulatory NetworksNeurology (clinical)NeuroinflammationBrain
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COMPUTED TOMOGRAPHY AND IMAGING FINDINGS OF CHRONIC OSTEOMYELITIS OF THE JAW.

2006

CT - OSTEOMYELITIS - JAW
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Cannabinoid CB1 receptors regulate neuronal TNF-α effects in experimental autoimmune encephalomyelitis.

2011

Abstract Cannabinoid CB1 receptors (CB1Rs) regulate the neurodegenerative damage of experimental autoimmune encephalomyelitis (EAE) and of multiple sclerosis (MS). The mechanism by which CB1R stimulation exerts protective effects is still unclear. Here we show that pharmacological activation of CB1Rs dampens the tumor necrosis factor α (TNFα)-mediated potentiation of striatal spontaneous glutamate-mediated excitatory postsynaptic currents (EPSCs), which is believed to cogently contribute to the inflammation-induced neurodegenerative damage observed in EAE mice. Furthermore, mice lacking CB1Rs showed a more severe clinical course and, in parallel, exacerbated alterations of sEPSC duration af…

Cannabinoid receptorEncephalomyelitis Autoimmune ExperimentalPolyunsaturated Alkamidesmedicine.medical_treatmentImmunologyExcitotoxicityGlutamic AcidArachidonic AcidsPharmacologyBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateReceptors Tumor Necrosis FactorAmidohydrolasesEtanerceptBehavioral Neurosciencechemistry.chemical_compoundMiceReceptor Cannabinoid CB1Fatty acid amide hydrolaseCannabinoid Receptor ModulatorsmedicineAnimalsDronabinolReceptors AMPA6-Cyano-7-nitroquinoxaline-23-dioneMice KnockoutNeuronsEndocrine and Autonomic SystemsTumor Necrosis Factor-alphaNeurodegenerationExperimental autoimmune encephalomyelitisExcitatory Postsynaptic PotentialsAnandamidemedicine.diseaseEndocannabinoid systemCorpus StriatumMice Inbred C57BLchemistryImmunoglobulin GImmunologyNerve DegenerationSettore MED/26 - NeurologiaFemaleCannabinoidDizocilpine MaleateEndocannabinoidsBrain, behavior, and immunity
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In Vivo Imaging of Partially Reversible Th17 Cell-Induced Neuronal Dysfunction in the Course of Encephalomyelitis

2010

SummaryNeuronal damage in autoimmune neuroinflammation is the correlate for long-term disability in multiple sclerosis (MS) patients. Here, we investigated the role of immune cells in neuronal damage processes in animal models of MS by monitoring experimental autoimmune encephalomyelitis (EAE) by using two-photon microscopy of living anaesthetized mice. In the brainstem, we detected sustained interaction between immune and neuronal cells, particularly during disease peak. Direct interaction of myelin oligodendrocyte glycoprotein (MOG)-specific Th17 and neuronal cells in demyelinating lesions was associated with extensive axonal damage. By combining confocal, electron, and intravital microsc…

Cell signalingPathologymedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalEncephalomyelitisImmunologyApoptosisCell CommunicationBiologyReceptors N-Methyl-D-AspartateMyelin oligodendrocyte glycoproteinMiceImmune systemCell MovementmedicineAnimalsImmunology and AllergyNeuroinflammationCells CulturedNeuronsMultiple sclerosisExperimental autoimmune encephalomyelitisInterleukin-17T-Lymphocytes Helper-Inducermedicine.diseaseAxonsCell biologyMice Inbred C57BLInfectious Diseasesnervous systemSynapsesbiology.proteinCalciumIntravital microscopyImmunity
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