Search results for "Autoimmunity"

showing 10 items of 349 documents

GFAPα IgG-associated encephalitis upon daclizumab treatment of MS

2018

ObjectiveTo describe a case of glial fibrillary acidic protein (GFAP)α immunoglobulin G (IgG)-associated encephalitis in a patient referred to us with MS on daclizumab treatment and to summarize characteristics of 5 additional recent German MS cases of serious encephalitis along with a previously published American case of CNS vasculitis associated with daclizumab.MethodsEvaluation of cause, clinical symptoms, and treatment response.ResultsThe 6 patients included 4 women and 2 men. The median age at onset was 38 years (range 32–51 years). Clinical presentation was marked by progressing neuropsychologic and/or neurologic deficits. Additional drug rash with eosinophilia was seen in 3 patients…

0301 basic medicine41132medicine.disease_causeArticleImmunoglobulin GAutoimmunity03 medical and health sciences0302 clinical medicineDaclizumabmedicineEosinophiliaPleocytosisbiologyGlial fibrillary acidic proteinbusiness.industrymedicine.disease030104 developmental biologyNeurologyImmunologybiology.proteinNeurology (clinical)medicine.symptomAntibodybusiness030217 neurology & neurosurgeryEncephalitismedicine.drugNeurology - Neuroimmunology Neuroinflammation
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Sex Alters the MHC Class I HLA-A Association With Polyglandular Autoimmunity.

2018

Abstract Context The major histocompatibility complex (MHC) strongly contributes to the development of polyglandular autoimmunity (PGA). Objective To evaluate the impact of sex on human leukocyte antigen (HLA) association with PGA for the first time. Design Cross-sectional immunogenetic study. Setting Academic tertiary referral Orphan Disease Center for PGA (ORPHA 282196) and immunogenetics laboratory. Subjects Patients (158) with coexistent type 1 diabetes and autoimmune thyroid disease (adult type 3 PGA, ORPHA 227982) and 479 unrelated healthy controls. Interventions All 637 white subjects were typed for HLA-A, -B, -DRB1, -DQA1, and -DQB1 alleles at a two-field level. Main Outcome Measure…

0301 basic medicineAdultMalemedicine.medical_specialtyEndocrinology Diabetes and MetabolismClinical Biochemistry030209 endocrinology & metabolismContext (language use)Human leukocyte antigenMajor histocompatibility complexmedicine.disease_causeBiochemistryAutoimmunity03 medical and health sciences0302 clinical medicineEndocrinologySex FactorsGene FrequencyInternal medicineMHC class ImedicineHumansGenetic Predisposition to DiseasePolyendocrinopathies AutoimmuneType 1 diabetesMHC class IIbiologyHLA-A Antigensbusiness.industryHistocompatibility TestingBiochemistry (medical)Histocompatibility Antigens Class IMiddle Agedmedicine.diseasePrognosisHLA-A030104 developmental biologyEndocrinologyCross-Sectional StudiesDiabetes Mellitus Type 1HaplotypesCase-Control Studiesbiology.proteinFemalebusinessBiomarkersFollow-Up StudiesThe Journal of clinical endocrinology and metabolism
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Body Mass Index and Associated Clinical Variables in Patients with Non-Celiac Wheat Sensitivity.

2019

Background: Non-Celiac Wheat Sensitivity (NCWS) is still a largely undefined condition, due to the lack of a diagnostic marker. Few data are available about the nutritional characteristics of NCWS patients at diagnosis. Aims: To evaluate the proportion of NCWS patients who were underweight, normal weight, overweight, or obese at diagnosis, and to search for possible correlations between their Body Mass Index (BMI) and other NCWS-related disease characteristics. Patients and Methods: The clinical charts of 145 NCWS patients (125 F, 20 M, mean age 37.1 &plusmn

0301 basic medicineAdultMalemedicine.medical_specialtySettore MED/09 - Medicina InternaClinical variablesHLA haplotypelcsh:TX341-641autoimmune diseaseAutoimmunityDiseaseWheat HypersensitivityOverweightBody Mass Index (BMI)GastroenterologyArticleBody Mass IndexCeliac Disease (CD)03 medical and health sciencesIrritable Bowel Syndrome (IBS)0302 clinical medicineThinnessWeight lossInternal medicineHLA-DQ AntigensmedicineHumansIn patientautoimmune diseasesIrritable bowel syndromeRetrospective StudiesNutrition and Dieteticsbusiness.industrynutritional and metabolic diseasesMiddle AgedOverweightmedicine.diseasePrognosis030104 developmental biologyHaplotypesnon-celiac wheat sensitivity (NCWS)030211 gastroenterology & hepatologyFemalemedicine.symptomUnderweightbusinesslcsh:Nutrition. Foods and food supplyBody mass indexFood ScienceNutrients
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From lymphopoiesis to plasma cells differentiation, the age-related modifications of B cell compartment are influenced by “inflamm-ageing”

2017

Ageing is a complex process characterized by a general decline in physiological functions with increasing morbidity and mortality. The most important aspect of ageing is the chronic inflammatory status, named “inflamm-ageing”, strictly associated with the deterioration of the immune function, termed “immunosenescence”. Both are causes of increased susceptibility of elderly to infectious diseases, cancer, dementia, cardiovascular diseases and autoimmunity, and of a decreased response to vaccination. It has been widely demonstrated that ageing has a strong impact on the remodelling of the B cell branch of immune system. The first evident effect is the significant decrease in circulati…

0301 basic medicineAgingImmunosenescenceHealth StatusPlasma CellsNaive B cellAutoimmunityInflammationBiologyLymphocyte ActivationBiochemistry03 medical and health sciences0302 clinical medicineImmune systemAntigenAge-related diseasemedicineAnimalsHumansLymphopoiesisProgenitor cellMolecular BiologyCellular SenescenceB cellInflammationB cellB-LymphocytesLymphopoiesisCell DifferentiationImmunosenescenceInflamm-ageing030104 developmental biologymedicine.anatomical_structureNeurologyImmune SystemImmunologyInflammation Mediatorsmedicine.symptomExhausted/Senescent cell030215 immunologyBiotechnologyAgeing Research Reviews
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Secretion of autoimmune antibodies in the human subcutaneous adipose tissue

2018

The adipose tissue (AT) contributes to systemic and B cell intrinsic inflammation, reduced B cell responses and secretion of autoimmune antibodies. In this study we show that adipocytes in the human obese subcutaneous AT (SAT) secrete several pro-inflammatory cytokines and chemokines, which contribute to the establishment and maintenance of local and systemic inflammation, and consequent suboptimal immune responses in obese individuals, as we have previously shown. We also show that pro-inflammatory chemokines recruit immune cells expressing the corresponding receptors to the SAT, where they also contribute to local and systemic inflammation, secreting additional pro-inflammatory mediators.…

0301 basic medicineB CellsPhysiologylcsh:MedicineAutoimmunityPathology and Laboratory MedicineSystemic inflammationWhite Blood CellsAnimal CellsImmune PhysiologyPlasma cell differentiationAdipocytesMedicine and Health Scienceslcsh:ScienceImmune ResponseConnective Tissue CellsInnate Immune SystemMultidisciplinaryT CellsBody Fluids3. Good healthBloodmedicine.anatomical_structurePhysiological ParametersConnective TissueCytokinesChemokinesCellular TypesAnatomymedicine.symptomResearch ArticleLipolysisImmune CellsImmunologySubcutaneous FatInflammationBiology03 medical and health sciencesSigns and SymptomsImmune systemAntigenDiagnostic MedicinemedicineHumansObesityAntibody-Producing CellsB cellAutoantibodiesInflammationBlood CellsTumor Necrosis Factor-alphalcsh:RBody WeightAutoantibodyBiology and Life SciencesGerminal centerCell BiologyMolecular DevelopmentOxidative StressBiological Tissue030104 developmental biologyImmune SystemImmunologylcsh:QTranscription FactorsDevelopmental BiologyPLOS ONE
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Mast cells contribute to autoimmune diabetes by releasing interleukin-6 and failing to acquire a tolerogenic IL-10+ phenotype

2017

Mast cells (MCs) are innate immune cells that exert positive and negative immune modulatory functions capable to enhance or limit the intensity and/or duration of adaptive immune responses. Although MCs are crucial to regulate T cell immunity, their action in the pathogenesis of autoimmune diseases is still debated. Here we demonstrate that MCs play a crucial role in T1D pathogenesis so that their selective depletion in conditional MC knockout NOD mice protects them from the disease. MCs of diabetic NOD mice are overly inflammatory and secrete large amounts of IL-6 that favors differentiation of IL-17-secreting T cells at the site of autoimmunity. Moreover, while MCs of control mice acquire…

0301 basic medicineBlood GlucoseAutoimmune diabeteAutoimmunityNodmedicine.disease_causeT-Lymphocytes RegulatoryAutoimmunityImmune toleranceSettore MED/13 - EndocrinologiaMiceAutoimmune diabetes0302 clinical medicineMice Inbred NODImmunology and AllergyNOD miceMice KnockoutInterleukin-17Forkhead Transcription FactorsFlow CytometryImmunohistochemistryhumanitiesInterleukin-10Interleukin 10Tumor necrosis factor alphaImmunologySettore MED/50 - Scienze Tecniche Mediche ApplicateMice TransgenicLaser Capture MicrodissectionReal-Time Polymerase Chain Reactionbehavioral disciplines and activities03 medical and health sciencesIslets of LangerhansImmune systemChymasesmedicineAnimalsInflammationInnate immune systembusiness.industryInterleukin-6Immune toleranceSettore MED/46 - Scienze Tecniche di Medicina di LaboratorioAutoimmune diabetes; Immune tolerance; Interleukin-10; Interleukin-6; Mast cells030104 developmental biologyDiabetes Mellitus Type 1ImmunologyMast cellsTh17 CellsMast cells; Autoimmune diabetes; Interleukin-6; Immune tolerance; Interleukin-10business030215 immunology
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EBI2 Is Highly Expressed in Multiple Sclerosis Lesions and Promotes Early CNS Migration of Encephalitogenic CD4 T Cells

2017

Arrival of encephalitogenic T cells at inflammatory foci represents a critical step in development of experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis. EBI2 and its ligand, 7{alpha},25-OHC, direct immune cell localization in secondary lymphoid organs. CH25H and CYP7B1 hydroxylate cholesterol to 7{alpha},25-OHC. During EAE, we found increased expression of CH25H by microglia and CYP7B1 by CNS-infiltrating immune cells elevating the ligand concentration in the CNS. Two critical pro-inflammatory cytokines, interleukin-23 (IL-23) and interleukin-1 beta (IL-1{beta}), maintained expression of EBI2 in differentiating Th17 cells. In line with this, EBI2 enhan…

0301 basic medicineCD4-Positive T-LymphocytesCentral Nervous SystemMaleGPR183Cancer ResearchEncephalomyelitis Autoimmune ExperimentalOxysterolCentral nervous systemInterleukin-1betaCytochrome P450 Family 7CH25HmicrogliaAutoimmunityBiologymedicine.disease_causemultiple sclerosisInterleukin-23General Biochemistry Genetics and Molecular BiologyAutoimmunityReceptors G-Protein-Coupled03 medical and health sciencesMiceImmune systemCell MovementmedicineAnimalsEBI2lcsh:QH301-705.5MicrogliaEAEMultiple sclerosisExperimental autoimmune encephalomyelitisGPR18325-OHCmedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)ImmunologySteroid HydroxylasesTh17 CellsFemaleTh17CNSoxysterolCell Reports
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Increased expression of interleukin-22 in patients with giant cell arteritis

2017

Objectives GCA is characterized by arterial remodelling driven by inflammation. IL-22 is an attractive cytokine which acts at the crosstalk between immune and stromal cells. We hypothesized that IL-22 might be induced in GCA and might be involved in disease pathogenesis. Methods Patients subjected to temporal artery biopsies (TABs) naive from therapy were enrolled: 27 biopsy-proven GCA, 8 biopsy-negative GCA, 21 biopsy-negative non-GCA patients. Expression of IL-22 was determined in TABs by immunohystochemistry, in plasma by ELISA, in peripheral blood mononuclear cells by real-time PCR and flow cytometry. Effects of IL-22 on viability and gene expression of primary cultures obtained from TA…

0301 basic medicineCD4-Positive T-LymphocytesMalearterial remodelling; autoimmunity; giant cell arteritis; inflammation; interleukin-22; pathogenesismedicine.medical_treatmentMessengerInterleukin 220302 clinical medicineimmune system diseasesarterial remodelling; autoimmunity; giant cell arteritis; inflammation; interleukin-22; pathogenesis; Aged; Aged 80 and over; CD4-Positive T-Lymphocytes; Calcium Ionophores; Carcinogens; Case-Control Studies; Enzyme-Linked Immunosorbent Assay; Female; Flow Cytometry; Giant Cell Arteritis; Humans; Immunohistochemistry; In Vitro Techniques; Interleukins; Ionomycin; Leukocytes Mononuclear; Male; RNA Messenger; Real-Time Polymerase Chain Reaction; Temporal Arteries; Tetradecanoylphorbol Acetate80 and overLeukocytesPharmacology (medical)skin and connective tissue diseasesAged 80 and overIonomycinpathogenesisautoimmunityInterleukinFlow CytometryImmunohistochemistryTemporal ArteriesCalcium IonophoresCytokinecardiovascular systemTetradecanoylphorbol AcetateFemalemedicine.symptomgiant cell arteritiStromal cellMononuclearGiant Cell ArteritisInflammationEnzyme-Linked Immunosorbent AssayIn Vitro TechniquesReal-Time Polymerase Chain ReactionPeripheral blood mononuclear cellarterial remodelling03 medical and health sciencesRheumatologymedicineHumansViability assayRNA Messengercardiovascular diseasesAged030203 arthritis & rheumatologybusiness.industryInterleukinsinterleukin-22medicine.diseaseGiant cell arteritis030104 developmental biologyinflammationCase-Control StudiesImmunologyCarcinogensLeukocytes MononuclearRNAbusiness
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The iNOS Activity During an Immune Response Controls the CNS Pathology in Experimental Autoimmune Encephalomyelitis

2019

Inducible nitric oxide synthase (iNOS) plays a critical role in the regulation of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Previous studies have shown that iNOS plays pathogenic as well as regulatory roles in MS and EAE. However, how does iNOS alters the pathophysiology of the central nervous system (CNS) in neuronal autoimmunity is not clearly understood. In the present work, we show that treatment of mice with L-NAME, an iNOS inhibitor, during the antigen-priming phase primarily alters brain pathology, while in the subsequent effector phase of the immune response, the spinal cord is involved. Inhibition of iNOS during the priming phase of the immune res…

0301 basic medicineCD4-Positive T-LymphocytesPathologyexperimental autoimmune encephalomyelitisNitric Oxide Synthase Type IIApoptosismedicine.disease_causeAutoimmunityMice0302 clinical medicineImmunology and AllergyEnzyme InhibitorsOriginal ResearchMice KnockoutbiologyExperimental autoimmune encephalomyelitisautoimmunityCell DifferentiationNitric oxide synthaseOligodendrogliamedicine.anatomical_structureNG-Nitroarginine Methyl EsterIntegrin alpha Mlcsh:Immunologic diseases. Allergymedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisLymphoid TissueCentral nervous systemImmunology03 medical and health sciencesInterferon-gammaImmune systemmedicineAnimalsHumansNOS2−/− neuroinflammationNeuroinflammationbusiness.industryMultiple sclerosisinducible nitric oxide synthaseDendritic Cellsmedicine.diseasecentral nervous systemMice Inbred C57BL030104 developmental biologybiology.proteinbusinesslcsh:RC581-607030215 immunologyGranulocytesFrontiers in Immunology
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The immunological implication of the new vitamin D metabolism

2018

Vitamin D is a neuro-hormone regulating calcium-phosphate homeostasis, cell proliferation, and immunomodulation. exogenous and endogenous Vitamin D is inactive, and two hydroxylations are required to produce the active hormone. The first hydroxylation is unique to the liver, while the second step occurs in kidney, brain, lung, prostate, placenta, and immune cells. Kidney-derived calcitriol regulates calcium homeostasis. active hormone produced by brain and immune cells mediates immune system response; lung calcitriol is involved in fighting respiratory tract infections; finally, prostate and placenta Vitamin D regulates cells growth and proliferation within such tissues. immune modulation b…

0301 basic medicineCalcitriolImmunologylcsh:Medicinevitamin Dmedicine.disease_causeimmunomodulationCalcitriol receptorAutoimmunity03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemCYPsCYPVitamin D and neurologyImmunology and AllergyMedicineVDRCalcium metabolismReview PaperInnate immune systembusiness.industryautoimmunitylcsh:R030104 developmental biologychemistryImmunologybusinessCholecalciferol030217 neurology & neurosurgerymedicine.drugCentral European Journal of Immunology
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