Search results for "immune disease"

showing 10 items of 359 documents

Defective expression of CD95 (FAS/APO-1) molecule suggests apoptosis impairment of T and B cells in HLA-B8, DR3-positive individuals.

1997

Activation-induced apoptosis is one of the primary control mechanisms for the negative selection of an immune response, leading to maintenance of immune homeostasis and selective T cell deletion. The interaction between the surface molecule Fas and its ligand (FasL) has been proposed as a primary mechanism initiating T cell apoptosis. The T cell receptor modulates the expression and function of these molecules. Defects in the Fas/FasL apoptosis pathway have been shown to result in autoimmune disease in humans and in murine models. Because subjects carrying the HLA-B8, DR3 haplotype show a number of immune dysfunctions, including membrano-proliferative glomerulonephritis, systemic lupus eryt…

CD3 ComplexT cellCD8 AntigensT-LymphocytesImmunologyAntigens CD19Lipopolysaccharide ReceptorsApoptosisBiologyFas ligandHLA-B8 AntigenImmune systemHLA-DR3 AntigenmedicineImmunology and AllergyCytotoxic T cellHumansfas ReceptorAutoimmune diseaseB-LymphocytesHistocompatibility TestingT-cell receptorGeneral Medicinemedicine.diseaseFas receptorFlow Cytometrymedicine.anatomical_structureApoptosisImmunologyCD4 AntigensCancer researchHuman immunology
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Gene therapy using IL 12 family members in infection, auto immunity, and cancer.

2009

Interleukin-12 (IL-12) is known for several years to have an essential role in inflammatory responses and innate resistance to infection and cancer. This has been largely attributed to its ability to initiate the differentiation of T-helper-1 (Th1) cells producing interferon-gamma. Recently, two new cytokines, IL-23 and IL-27, with homology to IL-12 were discovered and assigned to the IL-12 family of cytokines. Growing evidence supports a role for IL-23 as key mediator of autoimmune disease regulating the new Th17 subset of CD4+ T cells. IL-27 can have pro- and anti-inflammatory effects, which increase Th1 differentiation, suppress Th2 proliferation, or stimulate cytotoxic T cell activity. …

CD4-Positive T-Lymphocytesmedicine.medical_treatmentGenetic enhancementAutoimmunityBiologymedicine.disease_causeInfectionsInterleukin-23AutoimmunityAutoimmune DiseasesMiceImmunityNeoplasmsDrug DiscoveryGeneticsmedicineCytotoxic T cellAnimalsHumansMolecular BiologyGenetics (clinical)Autoimmune diseaseClinical Trials as TopicInterleukinsCancerGenetic TherapyTh1 Cellsmedicine.diseaseInterleukin-12CytokineImmunologyInterleukin 12Molecular MedicineTh17 CellsCurrent gene therapy
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Long-range DNA looping and gene expression analyses identify DEXI as an autoimmune disease candidate gene

2011

The chromosome 16p13 region has been associated with several autoimmune diseases, including type 1 diabetes (T1D) and multiple sclerosis (MS). CLEC16A has been reported as the most likely candidate gene in the region, since it contains the most disease-associated single-nucleotide polymorphisms (SNPs), as well as an imunoreceptor tyrosine-based activation motif. However, here we report that intron 19 of CLEC16A, containing the most autoimmune disease-associated SNPs, appears to behave as a regulatory sequence, affecting the expression of a neighbouring gene, DEXI. The CLEC16A alleles that are protective from T1D and MS are associated with increased expression of DEXI, and no other genes in …

Candidate geneQuantitative Trait LociSingle-nucleotide polymorphismBiologyPolymerase Chain ReactionPolymorphism Single NucleotideMonocytesAutoimmune Diseases03 medical and health sciences0302 clinical medicineGeneticsHumansEnhancerMolecular BiologyGeneGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesIntronMembrane ProteinsPromoterGeneral MedicineArticlesDNADNA-Binding ProteinsRegulatory sequenceCandidate Disease Gene030217 neurology & neurosurgeryChromosomes Human Pair 16Human Molecular Genetics
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Human Hsp10 and Early Pregnancy Factor (EPF) and their relationship and involvement in cancer and immunity: current knowledge and perspectives.

2009

This article is about Hsp10 and its intracellular and extracellular forms focusing on the relationship of the latter with Early Pregnancy Factor and on their roles in cancer and immunity. Cellular physiology and survival are finely regulated and depend on the correct functioning of the entire set of proteins. Misfolded or unfolded proteins can cause deleterious effects and even cell death. The chaperonins Hsp10 and Hsp60 act together inside the mitochondria to assist protein folding. Recent studies demonstrated that these proteins have other roles inside and outside the cell, either together or independently of each other. For example, Hsp10 was found increased in the cytosol of different t…

Cell physiologyHsp10 tumor immunity chaperonins early pregnancy factor developmentProgrammed cell deathProtein Foldingmedicine.medical_treatmentBiologyPregnancy ProteinsGeneral Biochemistry Genetics and Molecular BiologyAutoimmune DiseasesImmune systemImmunityNeoplasmsExtracellularmedicineChaperonin 10Suppressor Factors ImmunologicHumansGeneral Pharmacology Toxicology and PharmaceuticsSettore BIO/16 - Anatomia UmanaGrowth factorGeneral MedicineCell biologyMitochondriaProtein TransportHSP60IntracellularLife sciences
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Remission of experimental autoimmune hepatitis is associated with antigen-specific and non-specific immunosuppression.

1993

SUMMARY Experimental autoimmune hepatitis (EAH) is an animal model for autoimmune hepatitis. The disease is T cell-mediated and runs a subacute course, with maximal disease activity around week four after disease induction and a slow ensuing recovery. The aim of the present study was to investigate the immunoregulatory mechanisms that may account for recovery in EAH. It was found that T cell reactivity to liver antigens preceded histological disease, but at the peak of disease activity this T cell response was already suppressed. Active and antigen-specific suppression could be demonstrated, as irradiated splenocytes from animals at the beginning of recovery from EAH were able to suppress i…

Cellular immunitymedicine.medical_treatmentT-LymphocytesImmunologyAutoimmune hepatitisBiologyHepatitis AnimalAutoimmune DiseasesMiceImmune systemAntigenmedicineImmune ToleranceTetanus ToxoidImmunology and AllergyAnimalsAntigensAutoimmune diseaseHepatitisMice Inbred BALB CImmunosuppressionT lymphocytemedicine.diseaseMice Inbred C57BLImmunologyFemaleResearch Article
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Intrinsic TNFR2 signaling in T regulatory cells provides protection in CNS autoimmunity

2018

Significance In spite of TNF involvement in the pathogenesis of multiple sclerosis (MS), systemic TNF neutralization in MS patients was not successful. One of the possible reasons is that TNF possesses both pathogenic and protective features that may be related to TNFR1 versus TNFR2 receptor engagement. This study uncovers one of such protective functions of TNF mediated by intrinsic TNFR2 signaling in Treg cells. In mice bearing humanized TNF and TNFR2 genetic loci, TNFR2 ablation restricted to Treg cells led to reduced capacity to control Th17 cell responses, exacerbated experimental autoimmune encephalomyelitis (EAE) development, and affected the maintenance of Treg cells. These findings…

Central Nervous System0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT regulatory cellsmedicine.medical_treatmentAutoimmunitychemical and pharmacologic phenomenaBiologymedicine.disease_causeT-Lymphocytes RegulatoryneuroinflammationAutoimmunityMice03 medical and health sciencesImmunology and Inflammation0302 clinical medicineImmune systemmedicineAnimalsHumansReceptors Tumor Necrosis Factor Type IIIL-2 receptorCells CulturedNeuroinflammationMice KnockoutAutoimmune diseaseMultidisciplinaryEAETumor Necrosis Factor-alphaExperimental autoimmune encephalomyelitisFOXP3hemic and immune systemsBiological Sciencesmedicine.diseaseTNF/TNFR2Mice Inbred C57BLDisease Models Animalhumanized mice030104 developmental biologyCytokineGene Expression RegulationImmunology030215 immunologyProceedings of the National Academy of Sciences
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Myeloid Cells in the Central Nervous System

2017

The central nervous system (CNS) and its meningeal coverings accommodate a diverse myeloid compartment that includes parenchymal microglia and perivascular macrophages, as well as choroid plexus and meningeal macrophages, dendritic cells, and granulocytes. These myeloid populations enjoy an intimate relationship with the CNS, where they play an essential role in both health and disease. Although the importance of these cells is clearly recognized, their exact function in the CNS continues to be explored. Here, we review the subsets of myeloid cells that inhabit the parenchyma, meninges, and choroid plexus and discuss their roles in CNS homeostasis. We also discuss the role of these cells in…

Central Nervous System0301 basic medicinePathologymedicine.medical_specialtyMyeloidNeuroimmunomodulationImmunologyCentral nervous systemBiologyInfectionsmedicine.disease_causeNeuroprotectionArticleAutoimmune DiseasesAutoimmunity03 medical and health sciencesMeningesmedicineAnimalsHumansImmunology and AllergyMyeloid CellsMicrogliaNeurodegenerationMeningesNeurodegenerative Diseasesmedicine.diseaseNeuroprotection030104 developmental biologyInfectious Diseasesmedicine.anatomical_structureChoroid PlexusImmunologyWounds and InjuriesChoroid plexusImmunity
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Direct suppression of CNS autoimmune inflammation via the cannabinoid receptor CB1 on neurons and CB2 on autoreactive T cells.

2007

The cannabinoid system is immunomodulatory and has been targeted as a treatment for the central nervous system (CNS) autoimmune disease multiple sclerosis. Using an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), we investigated the role of the CB(1) and CB(2) cannabinoid receptors in regulating CNS autoimmunity. We found that CB(1) receptor expression by neurons, but not T cells, was required for cannabinoid-mediated EAE suppression. In contrast, CB(2) receptor expression by encephalitogenic T cells was critical for controlling inflammation associated with EAE. CB(2)-deficient T cells in the CNS during EAE exhibited reduced levels of apoptosis, a higher…

Central Nervous SystemCannabinoid receptorEncephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentEncephalomyelitisT-LymphocytesInflammationApoptosisMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyReceptor Cannabinoid CB2MiceReceptor Cannabinoid CB1medicineCannabinoid receptor type 2AnimalsCell ProliferationDNA PrimersAutoimmune diseaseNeuronsExperimental autoimmune encephalomyelitisGeneral Medicinemedicine.diseaseEndocannabinoid systemImmunohistochemistryImmunologyEncephalitislipids (amino acids peptides and proteins)Cannabinoidmedicine.symptomNature medicine
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Role of Sortilin in Models of Autoimmune Neuroinflammation

2015

Abstract The proneurotrophin receptor sortilin is a protein with dual functions, being involved in intracellular protein transport, as well as cellular signal transduction. The relevance of the receptor for various neuronal disorders, such as dementia, seizures, and brain injury, is well established. In contrast, little is known about the role of sortilin in immune cells and inflammatory diseases. The aim of our study was to elucidate the distribution of sortilin in different immune cell types in mice and humans and to analyze its function in autoimmune CNS inflammation. Sortilin was expressed most profoundly in murine and human macrophages and dendritic cells and to a much lesser extent in…

Central Nervous SystemCell typeEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisT-LymphocytesEncephalomyelitisImmunologyAutoimmunityBiologyMiceImmune systemmedicineAnimalsHumansImmunology and AllergyReceptorNeuroinflammationMice KnockoutAutoimmune diseaseAntigen PresentationMacrophagesExperimental autoimmune encephalomyelitisDendritic Cellsmedicine.diseaseImmunity InnateMice Inbred C57BLAdaptor Proteins Vesicular TransportBrain InjuriesImmunologyNeurogenic InflammationSignal transductionSignal Transduction
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The Relationship between Gray Matter Quantitative MRI and Disability in Secondary Progressive Multiple Sclerosis

2016

Purpose: In secondary progressive Multiple Sclerosis (SPMS), global neurodegeneration as a driver of disability gains importance in comparison to focal inflammatory processes. However, clinical MRI does not visualize changes of tissue composition outside MS lesions. This quantitative MRI (qMRI) study investigated cortical and deep gray matter (GM) proton density (PD) values and T1 relaxation times to explore their potential to assess neuronal damage and its relationship to clinical disability in SPMS. Materials and Methods: 11 SPMS patients underwent quantitative T1 and PD mapping. Parameter values across the cerebral cortex and deep GM structures were compared with 11 healthy controls, and…

Central Nervous SystemMalePathologyPhysiologylcsh:MedicinePathology and Laboratory MedicineNervous SystemBrain mappingDiagnostic Radiology030218 nuclear medicine & medical imaging0302 clinical medicineThalamusMedicine and Health SciencesRelaxation TimeMedicineGray Matterlcsh:ScienceCerebrospinal FluidCerebral CortexMultidisciplinarymedicine.diagnostic_testRadiology and ImagingPhysicsPutamenNeurodegenerationBrainNeurodegenerative DiseasesMultiple Sclerosis Chronic ProgressiveMagnetic Resonance ImagingBody Fluidsmedicine.anatomical_structureNeurologyCerebral cortexPhysical SciencesFemaleAnatomyResearch ArticleAdultmedicine.medical_specialtyMultiple SclerosisImaging TechniquesImmunologyCentral nervous systemThalamusResearch and Analysis MethodsAutoimmune Diseases03 medical and health sciencesSigns and SymptomsDiagnostic MedicineIntellectual DisabilityHumansddc:610Relaxation (Physics)business.industryMultiple sclerosislcsh:RBiology and Life SciencesMagnetic resonance imagingmedicine.diseaseDemyelinating DisordersCase-Control StudiesLesionslcsh:QClinical ImmunologyClinical Medicinebusiness030217 neurology & neurosurgeryPLOS ONE
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