Search results for "AUTOIMMUNE DISEASES"

showing 10 items of 210 documents

Use of a clinicoradiological score to determine the presurgical diagnosis of autoimmune hypophysitis in a teenage girl.

2013

The distinction between autoimmune hypophysitis and other non–hormone secreting pituitary masses is often difficult to determine with certainty without pituitary biopsy and pathological examination. To aid in this distinction, the authors recently published a clinicoradiological scoring system, which they used in the case of a 15-year-old girl presented here. The patient presented with headache, visual field defects, polydipsia, and polyuria, and she was found to have secondary hypogonadism and hypoadrenalism. Magnetic resonance imaging showed a pituitary mass of approximately 2 cm in diameter. Application of the clinicoradiological parameters gave a score of −6, which favored a diagnosis o…

Pituitary glandmedicine.medical_specialtyPathologyAdenomaAdolescentHypophysitisPrednisoloneAnti-Inflammatory AgentsHypopituitarismHypopituitarismAutoimmune DiseasesPolyuriaHypoadrenalismmedicineHumansbusiness.industryHeadacheGeneral Medicinemedicine.diseaseMagnetic Resonance ImagingRadiographyPituitary Hormonesmedicine.anatomical_structureTreatment OutcomePituitary GlandAutoimmune hypophysitisPrednisoloneFemaleRadiologymedicine.symptombusinessmedicine.drugJournal of neurosurgery. Pediatrics
researchProduct

Compromised central tolerance of ICA69 induces multiple organ autoimmunity

2014

For reasons not fully understood, patients with an organ-specific autoimmune disease have increased risks of developing autoimmune responses against other organs/tissues. We identified ICA69, a known β-cell autoantigen in Type 1 diabetes, as a potential common target in multi-organ autoimmunity. NOD mice immunized with ICA69 polypeptides exhibited exacerbated inflammation not only in the islets, but also in the salivary glands. To further investigate ICA69 autoimmunity, two genetically modified mouse lines were generated to modulate thymic ICA69 expression: the heterozygous ICA69(del/wt) line and the thymic medullary epithelial cell-specific deletion Aire-ΔICA69 line. Suboptimal central neg…

Primary Sjogren's syndromeGenetically modified mouseImmunologyThyroid GlandAutoimmune diabeteMice TransgenicThymus GlandBiologymedicine.disease_causeAutoantigensArticleSalivary GlandsSettore MED/13 - EndocrinologiaAutoimmune DiseasesAutoimmunityImmune toleranceAutoimmune thyroiditisIslets of LangerhansMiceICA69Mice Inbred NODImmune TolerancemedicineAnimalsImmunology and AllergyThymuAutoimmune thyroiditiNOD miceInflammationAutoimmune diseaseStomachmedicine.diseaseGene Expression RegulationAutoimmune polyendocrine syndromeImmunologyAutoimmune polyendocrine syndromeCentral toleranceJournal of Autoimmunity
researchProduct

In Vitro Phenotypic, Genomic and Proteomic Characterization of a Cytokine-Resistant Murine β-TC3 Cell Line

2012

Type 1 diabetes mellitus (T1DM) is caused by the selective destruction of insulin-producing β-cells. This process is mediated by cells of the immune system through release of nitric oxide, free radicals and pro-inflammatory cytokines, which induce a complex network of intracellular signalling cascades, eventually affecting the expression of genes involved in β-cell survival. The aim of our study was to investigate possible mechanisms of resistance to cytokine-induced β-cell death. To this purpose, we created a cytokine-resistant β-cell line (β-TC3R) by chronically treating the β-TC3 murine insulinoma cell line with IL-1β + IFN-γ. β-TC3R cells exhibited higher proliferation rate and resistan…

ProteomicsAnatomy and Physiologymedicine.medical_treatmentCell Culture Techniqueslcsh:MedicineApoptosisSettore MED/13 - EndocrinologiaMiceEndocrinologyImmune PhysiologyInsulin-Secreting CellsMolecular Cell BiologySOCS3lcsh:ScienceMultidisciplinaryCell DeathDiabetes mellitus cytokines. apoptosis SUMO4 NF-kBCell CycleNF-kappa BGenomicsCell cycleImmunohistochemistryCell biologyPhenotypeCytokineMedicineCytokinesResearch ArticleProgrammed cell deathCell SurvivalImmunologyDown-RegulationBiologyAutoimmune DiseasesCell LineDownregulation and upregulationmedicineAnimalsGene SilencingBiologyCell ProliferationDiabetic EndocrinologyEndocrine PhysiologyCell growthlcsh:RCell cultureApoptosisImmune SystemClinical ImmunologyInsulinomalcsh:QPLoS ONE
researchProduct

The Autoimmune Regulator AIRE in Thymoma Biology: Autoimmunity and Beyond

2010

Thymomas are tumors of thymic epithelial cells. They associate more often than any other human tumors with various autoimmune diseases; myasthenia gravis is the commonest, occurring in 10-50% of thymoma patients, depending on the World Health Organization-defined histologic subtype. Most thymomas generate many polyclonal maturing T lymphocytes but in disorganized microenvironments Failure to induce self-tolerance may be a key factor leading to the export of potentially autoreactive CD4 progeny, thus predisposing to autoimmune diseases. Normally, the master Autoimmune Regulator promotes expression of peripheral tissue-restricted antigens such as insulin by medullary thymic epithelial cells a…

Pulmonary and Respiratory MedicineThymomaThymomamedicine.medical_treatmentAutoimmunitymedicine.disease_causeWorld healthAutoimmune DiseasesAutoimmunityAntigenAIREhemic and lymphatic diseasesAPS-1HumansMedicineMyasthenia gravisbusiness.industryInsulinThymus NeoplasmsAutoimmune regulatormedicine.diseaseMyasthenia gravisOncologyImmunologybusinessAPECEDTranscription FactorsJournal of Thoracic Oncology
researchProduct

Cross-Reactivity of Antibodies Immunoadsorbed to Laminin with Recombinant Human La (SS-B) Protein

1998

Anti-La (SS-B) antibodies cross-reacting with mouse B1 laminin were reported in sera of patients with systemic lupus erythematosus. However, the common epitope had not been characterized. Immunoblotting conditions were established, allowing detection and elution of anti-La (SS-B)/laminin cross-reacting antibodies. Antibodies adsorbed to mouse B1 laminin represented a subclass of anti-La antibodies. They strongly reacted with human full length recombinant La protein. However, they failed to react with either an N-terminal La peptide consisting of amino acids 1-192 or a C-terminal La peptide starting at methionine 223, while they still reacted with recombinant La peptides consisting of the am…

Recombinant Fusion ProteinsMolecular Sequence DataImmunologyPeptideCross ReactionsBiologyAutoantigensEpitopeAutoimmune Diseaseslaw.inventionEpitopesMiceSpecies SpecificityAntigenAntibody SpecificitylawLamininConsensus SequenceAnimalsHumansImmunology and AllergyAmino Acid SequenceElméleti orvostudományokPeptide sequenceImmunosorbent TechniquesAutoantibodieschemistry.chemical_classificationOrvostudományokMolecular biologyPeptide FragmentsAmino acidRibonucleoproteinschemistryRecombinant DNAbiology.proteinKidney DiseasesLamininAntibodyJournal of Autoimmunity
researchProduct

Cutting Edge: Trans-Signaling via the Soluble IL-6R Abrogates the Induction of FoxP3 in Naive CD4+CD25− T Cells

2007

Abstract Chronic inflammatory diseases may develop when regulatory T cells (Tregs) fail to control the balance between tolerance and immunity. Alternatively, activated immune cells might prevent the induction or activation of Tregs in such diseases. In this study, we demonstrate that trans-signaling into T cells via the soluble IL-6 receptor completely abrogates the de novo induction of adaptive Tregs. Mechanistically, IL-6 trans-signaling augmented the expression of the TGF-β signaling inhibitor SMAD7. Consequently, SMAD7 overexpression in T cells using newly created transgenic mice rendered CD4+CD25− T cells resistant to the induction of FoxP3. Finally, IL-6 trans-signaling inhibited Treg…

Regulatory T cellImmunologyMice Transgenicchemical and pharmacologic phenomenaMice SCIDBiologyT-Lymphocytes RegulatoryAutoimmune DiseasesSmad7 ProteinMiceInterleukin 21Immune systemTransforming Growth Factor betaImmunitymedicineAnimalsHumansImmunology and AllergyCytotoxic T cellIL-2 receptorInflammationMice Inbred BALB CInterleukin-6ZAP70FOXP3Forkhead Transcription FactorsColitisReceptors Interleukin-6Cell biologyDisease Models Animalmedicine.anatomical_structureGene Expression RegulationChronic DiseaseImmunologySignal TransductionThe Journal of Immunology
researchProduct

Neuroinflammation by cytotoxic T-lymphocytes impairs retrograde axonal transport in an oligodendrocyte mutant mouse.

2012

Mice overexpressing proteolipid protein (PLP) develop a leukodystrophy-like disease involving cytotoxic, CD8+ T-lymphocytes. Here we show that these cytotoxic T-lymphocytes perturb retrograde axonal transport. Using fluorogold stereotactically injected into the colliculus superior, we found that PLP overexpression in oligodendrocytes led to significantly reduced retrograde axonal transport in retina ganglion cell axons. We also observed an accumulation of mitochondria in the juxtaparanodal axonal swellings, indicative for a disturbed axonal transport. PLP overexpression in the absence of T-lymphocytes rescued retrograde axonal transport defects and abolished axonal swellings. Bone marrow tr…

Retinal Ganglion CellsProteolipid protein 1MouseCD8-Positive T-LymphocytesGranzymesMyelinMiceBone Marrow TransplantationNeuronsddc:616MultidisciplinarybiologyQRNeurodegenerative DiseasesAnimal ModelsCell biologyOligodendrogliamedicine.anatomical_structureNeurologyMedicineResearch ArticleHeterozygoteMultiple SclerosisProteolipidsScienceImmunologyMice Transgenicchemical and pharmacologic phenomenaAutoimmune DiseasesModel OrganismsmedicineAnimalsBiologyNeuroinflammationInflammationImmunityDemyelinating DisordersOligodendrocyteAxonsGranzyme BPerforinGranzymenervous systemImmune SystemImmunologyMutationAxoplasmic transportbiology.proteinClinical ImmunologyMolecular NeuroscienceT-Lymphocytes CytotoxicNeurosciencePLoS ONE
researchProduct

Heat Shock Protein-60 and Risk for Cardiovascular Disease

2011

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. There is growing evidence that molecularchaperones, many of which are heat shock proteins HSPs, are involved in CVD pathogenesis. In this review we focus on HSP60,the human mitochondrial chaperone that also displays extramitochondrial and extracellular functions. HSP60 is typically cytoprotectivebut a number of stress conditions determine its conversion to a potentially toxic molecule for cells and tissues. We present illustrative examplesof specific subtypes of CVD where HSP60 is implicated in the initiation and/or progression of disease. The data not only indicatea pathogenic role for HSP60 but also its …

Riskanimal structuresChaperonin Heat shock protein-60 cardiomyocytes heart failure cardiovascular diseases atherosclerosisChaperonin heat shock protein 60 cardiomyocytes heart failure cardiovascular disease atherosclerosis apoptosis microRNAs (miRs) diabetes Atrial fibrillationApoptosischemical and pharmacologic phenomenaDiseaseBioinformaticsAutoimmune DiseasesPathogenesisHeat shock proteinAtrial FibrillationDrug DiscoveryExtracellularAnimalsHumansMyocytes CardiacHeart FailurePharmacologybiologyfungiChaperonin 60AtherosclerosisResponse to treatmentCardiovascular DiseasesReperfusion InjuryChaperone (protein)HypertensionImmunologybiology.proteinHSP60Stress conditionsBiomarkersCurrent Pharmaceutical Design
researchProduct

Intracellular osteopontin protects from autoimmunity-driven lymphoma development inhibiting TLR9-MYD88-STAT3 signaling

2022

Abstract Background Autoimmune disorders, including Systemic Lupus Erythematosus (SLE), are associated with increased incidence of hematological malignancies. The matricellular protein osteopontin (OPN) has been linked to SLE pathogenesis, as SLE patients show increased serum levels of OPN and often polymorphisms in its gene. Although widely studied for its pro-tumorigenic role in different solid tumours, the role of OPN in autoimmunity-driven lymphomagenesis has not been investigated yet. Methods To test the role of OPN in the SLE-associated lymphomagenesis, the SLE-like prone Faslpr/lpr mutation was transferred onto an OPN-deficient background. Spleen from Faslpr/lpr and OPN-/-Faslpr/lpr …

STAT3 Transcription FactorMice Inbred MRL lprCancer ResearchLymphomaSettore MED/08 - Anatomia PatologicaAutoimmune DiseasesMice Inbred C57BLAutoimmunity Diffuse large B cell lymphoma OsteopontinMiceOncologyToll-Like Receptor 9Myeloid Differentiation Factor 88HumansAnimalsLupus Erythematosus SystemicSettore MED/05 - Patologia ClinicaMolecular MedicineSignal TransductionAdaptor Proteins Signal TransducingMolecular Cancer
researchProduct

Clinical manifestations of the anti-IgLON5 disease

2017

Objective:To report the presentation, main syndromes, human leukocyte antigen (HLA) association, and immunoglobulin G (IgG) subclass in the anti-IgLON5 disease: a disorder with parasomnias, sleep apnea, and IgLON5 antibodies.Methods:This was a retrospective clinical analysis of 22 patients. The IgG subclass was determined using reported techniques.Results:Patients' median age was 64 years (range 46–83). Symptoms that led to initial consultation included sleep problems (8 patients; 36%), gait abnormalities (8; 36%), bulbar dysfunction (3; 14%), chorea (2; 9%), and cognitive decline (1; 5%). By the time of diagnosis of the disorder, 4 syndromes were identified: (1) a sleep disorder with paras…

Sleep Wake Disorders0301 basic medicinemedicine.medical_specialtyCell Adhesion Molecules NeuronalPopulationExcessive daytime sleepinessAutoimmune DiseasesProgressive supranuclear palsy03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansCognitive declineeducationAgedAutoantibodiesRetrospective StudiesAged 80 and overeducation.field_of_studySleep disorderbusiness.industryBrainSleep apneaChoreaParasomniaMiddle Agedmedicine.disease030104 developmental biologyImmunoglobulin GImmunotherapyNeurology (clinical)medicine.symptomCarrier ProteinsbusinessBiomarkers030217 neurology & neurosurgeryHLA-DRB1 ChainsNeurology
researchProduct