Search results for "Allergy"

showing 10 items of 3181 documents

Reply to: Safety and efficacy of secukinumab treatment in a patient with ankylosing spondylitis and concomitant multiple sclerosis: A commentary

2021

No abstract available

Multiple SclerosisRheumatologyAntirheumatic AgentsMultiple SclerosiImmunologyAntirheumatic AgentHumansImmunology and AllergySpondylitis AnkylosingAntibodies Monoclonal HumanizedHuman
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Role of apoptosis in autoimmunity.

2004

Autoimmune diseases are characterized by the activity of autoreactive lymphocytes that produce antibodies targeting self tissue or organ for destruction. Although the pathogenesis of these diseases is poorly understood, during the past two decades basic research has indicated apoptosis as the pivotal molecular mechanism leading to autoimmunity. Recently cytokines have been invoked in the regulation of the apoptosis-related factors and death receptors in autoimmune target destruction. These research advances have contributed to the identification of mechanisms controlling autoimmunity for defining novel therapeutic strategies.

Multiple SclerosisbiologyImmunologyThyroiditis AutoimmuneApoptosisAutoimmunitymedicine.disease_causeapoptosiGraves DiseaseAutoimmunityAutoimmune DiseasesPathogenesisDiabetes Mellitus Type 1Basic researchApoptosisImmunologybiology.proteinMolecular mechanismmedicineImmunology and AllergyDeath ReceptorsAnimalsHumansAntibodyJournal of clinical immunology
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ID: 186

2015

In the past years, and clear pathogenic role was shown for Th17 cells in the development of autoimmune diseases. In particular, these cells were shown to play a critical roIn the past years, and clear pathogenic role was shown for Th17 cells in the development of autoimmune diseases. In particular, these cells were shown to play a critical role in the development of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. One of the major cytokines Th17 cells produce is IL-17A, a cytokine of the IL-17 family. IL-17A, as well as it homologue IL-17F bind and trigger cells via the IL-17 receptor A/C complex. We have used a series of mice with deficiencies in the…

Multiple sclerosismedicine.medical_treatmentImmunologyExperimental autoimmune encephalomyelitisHematologyBiologymedicine.diseasemedicine.disease_causeBiochemistryAutoimmunityCytokineImmunologymedicineImmunology and AllergyInterleukin 17ReceptorMolecular BiologyTranscription factorFunction (biology)Cytokine
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NFAT1 deficit and NFAT2 deficit attenuate EAE via different mechanisms

2015

EAE serves as an animal model for multiple sclerosis and is initiated by autoreactive T cells that infiltrate the CNS. Recognition of myelin-associated Ags within the CNS leads to activation of the transcription factor family NFAT. Here, we demonstrate an essential role for NFAT in disease induction, as the combined lack of NFAT1 (NFATc2) and NFAT2 (NFATc1) completely protected mice. Single deficiency of either NFAT1 or NFAT2 ameliorated the course of EAE, and NFAT2 ablation resulted in an obstructed proinflammatory reaction. However, NFAT1 deficit led to an anti-inflammatory response with nonpathogenic Th17 and Th2 cells concurrently secreting IL-17, IL-4, and IL-10. Both IL-4 and IL-10 co…

Multiple sclerosismedicine.medical_treatmentImmunologyLymphokineImmunosuppressionNFATBiologymedicine.diseasemedicine.disease_causeAutoimmunityBlockadeProinflammatory cytokineImmunologymedicineImmunology and AllergyTranscription factorEuropean Journal of Immunology
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The Relapsing Polychondritis Disease Activity Index: Development of a disease activity score for relapsing polychondritis.

2012

Abstract Objective The rarity of relapsing polychondritis (RP) has hindered the development of standardized tools for clinical assessment. Here, we describe the development of a preliminary score for disease assessing activity in RP, the Relapsing Polychondritis Disease Activity Index (RPDAI). Methods Twenty-seven RP experts participated in an international collaboration. Selection and definition of items for disease activity were established by consensus during a 4-round internet-based Delphi survey. Twenty-six experts assessed the Physician's Global Assessment (PGA) of disease activity on 43 test cases on a 0–100 scale, yielding a total of 1118 PGA ratings. The weight of each item was est…

Multivariate statisticsmedicine.medical_specialtybusiness.industryImmunologyDelphi methodDiseasemedicine.diseaseSeverity of Illness IndexGeeInternal medicineSeverity of illnessPhysical therapyImmunology and AllergyMedicineHumansPolychondritis RelapsingbusinessGeneralized estimating equationRelapsing polychondritisRare disease
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Adoptive CD8 T Cell Control of Pathogens Cannot Be Improved by Combining Protective Epitope Specificities

2008

Adoptive transfer of CD8 T cells has the potential to cure infectious or malignant diseases that are refractory to conventional chemotherapy. A practically important but still unanswered question is whether mixtures of protective CD8 T cells with different epitope specificities mediate more efficient effector cell functions than do the monospecific individual CD8 T cell populations. In this study, we have addressed this issue for models of viral and bacterial infection. CD8 T cell-mediated cytotoxicity in vitro and protection in vivo were assessed to test whether CD8 T cell lines cooperate in target cell lysis and control of infection, respectively. Our data clearly show that mixtures of cy…

MuromegalovirusAdoptive cell transferT cellEpitopes T-LymphocyteBacteremiaStreptamerCD8-Positive T-LymphocytesBiologyEpitopeMicemedicineAnimalsImmunology and AllergyCytotoxic T cellViremiaAntigen-presenting cellT lymphocyteAdoptive TransferListeria monocytogenesVirologyDisease Models AnimalInfectious Diseasesmedicine.anatomical_structureCytomegalovirus InfectionsImmunologyFemaleCD8The Journal of Infectious Diseases
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Excessive CpG 1668 stimulation triggers IL-10 production by cDC that inhibits IFN-alpha responses by pDC.

2008

Upon stimulation with a wide range of concentrations of CpG oligodeoxynucleotide 2216 (CpG 2216), plasmacytoid DC are induced to produce type I IFN (IFN-alpha/beta). In contrast, CpG 1668 shows a bell-shaped dose-response correlation, i.e. only intermediate but not high doses of CpG 1668 induce IFN-alpha/beta. Interestingly, high-dose CpG 1668 completely inhibited IFN-alpha responses induced by CpG 2216. Experiments using supernatant of high-dose CpG-1668-treated cells indicated that secreted inhibitor(s) mediated the IFN-alpha shut-off. Among modulating cytokines, IL-10 turned out to be one important negative regulator. In line with this, supernatants of IL-10-deficient DC cultures stimula…

MuromegalovirusCpG OligodeoxynucleotideImmunologyStimulationmedicine.disease_causeNegative regulatorAutoimmunityMiceAdjuvants ImmunologicmedicineImmunology and AllergyAnimalsCells CulturedbiologyTLR9Interferon-alphaDendritic Cellsbiology.organism_classificationMolecular biologyInterleukin-10Interleukin 10CpG siteOligodeoxyribonucleotidesVesicular stomatitis virusToll-Like Receptor 9ImmunologyCytokinesEuropean journal of immunology
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Major Histocompatibility Complex Class I Allele-specific Cooperative and Competitive Interactions between Immune Evasion Proteins of Cytomegalovirus

2002

Cytomegaloviruses (CMVs) deploy a set of genes for interference with antigen presentation in the major histocompatibility complex (MHC) class I pathway. In murine CMV (MCMV), three genes were identified so far: m04/gp34, m06/gp48, and m152/gp40. While their function as immunoevasins was originally defined after their selective expression, this may not necessarily reflect their biological role during infection. The three immunoevasins might act synergistically, but they might also compete for their common substrate, the MHC class I complexes. To approach this question in a systematic manner, we have generated a complete set of mutant viruses with deletions of the three genes in all seven pos…

Muromegalovirusmurine cytomegalovirusImmunologyAntigen presentationGenes MHC Class IMutagenesis (molecular biology technique)Context (language use)Virus ReplicationMajor histocompatibility complexPolymerase Chain ReactionArticleMiceViral ProteinsMuromegalovirusMHC class IEscherichia coliAnimalsImmunology and AllergyGeneAllelesBACimmune evasionGlycoproteinsGeneticsMice Inbred BALB CMembrane GlycoproteinsbiologyalleleFibroblastsbiology.organism_classificationViral replicationMHC class IIbiology.proteinCarrier ProteinsJournal of Experimental Medicine
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Variation in RNA virus mutation rates across host cells.

2014

It is well established that RNA viruses exhibit higher rates of spontaneous mutation than DNA viruses and microorganisms. However, their mutation rates vary amply, from 10−6 to 10−4 substitutions per nucleotide per round of copying (s/n/r) and the causes of this variability remain poorly understood. In addition to differences in intrinsic fidelity or error correction capability, viral mutation rates may be dependent on host factors. Here, we assessed the effect of the cellular environment on the rate of spontaneous mutation of the vesicular stomatitis virus (VSV), which has a broad host range and cell tropism. Luria-Delbrück fluctuation tests and sequencing showed that VSV mutated similarly…

Mutation ratevirusesVirus Replicationmedicine.disease_causeMice[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesCricetinaeBaby hamster kidney celllcsh:QH301-705.50303 health sciencesMutation[SDV.MHEP.ME]Life Sciences [q-bio]/Human health and pathology/Emerging diseases030302 biochemistry & molecular biology3. Good healthViral evolution[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyResearch Articlelcsh:Immunologic diseases. Allergy[SDE.MCG]Environmental Sciences/Global ChangesImmunologyBiologyMicrobiologyEvolution Molecular03 medical and health sciences[SDV.EE.ECO]Life Sciences [q-bio]/Ecology environment/EcosystemsCell Line TumorVirologyGeneticsmedicineAnimalsBiologyMolecular BiologyTropism030304 developmental biology[SDV.EE.SANT]Life Sciences [q-bio]/Ecology environment/HealthEvolutionary BiologyPoint mutationRNA virusVesiculovirusbiology.organism_classificationVirologyMolecular biology[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyViral replicationlcsh:Biology (General)MutationMicrobial EvolutionParasitology[SDE.BE]Environmental Sciences/Biodiversity and Ecologylcsh:RC581-607Population GeneticsPLoS Pathogens
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Definitive Link of Mutation c.351delC and Development of Hereditary Angioedema in a Large Brazilian Family

2011

S U N D A Y 381 Definitive Link of Mutation c.351delC and Development of Hereditary Angioedema in a Large Brazilian Family M. F. Ferraro, A. S. Moreno, E. Castelli, A. P. Lange, E. A. Donadi, K. Bork, W. Sarti, L. K. Arruda; School of Medicine of Ribeirao Preto, Ribeirao Preto, BRAZIL, Johannes-Gutenberg University, Mainz, GERMANY. RATIONALE:We have previously described the identification of a novel SERPING1 mutation (c.351delC) in members of a large Brazilian family with Hereditary Angioedema (HAE). In the present study, we have aimed to verify the association of this mutation with the development of HAE in this family. METHODS: Family pedigree was constructed with 275 individuals distribu…

MutationAbdominal painPediatricsmedicine.medical_specialtybiologyAngioedemabusiness.industryImmunologyDiseasemedicine.disease_causemedicine.diseaseAsymptomaticC1-inhibitorExonHereditary angioedemabiology.proteinImmunology and AllergyMedicinemedicine.symptombusinessJournal of Allergy and Clinical Immunology
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