Search results for "interleukin"

showing 10 items of 1856 documents

Comparison of salivary cytokines levels among individuals with Down syndrome, cerebral palsy and normoactive

2019

Background Individuals with Down syndrome (DS) present increased susceptibility to infections and high prevalence of periodontal disease. The objective of this study is to evaluate the salivary concentrations of IL-1β, IL-6, IL-8, IL-10, TNFα and IL-12p70 of DS individuals and compare to cerebral palsy (CP) and normoactive patients (all with gingivitis). Material and Methods Twenty-two individuals with DS, 24 with CP and 22 normoactive participated in this cross-sectional study. Salivary flow rate, osmolality rate, Oral Hygiene Index, Gingival Index (GI) and salivary inflammatory markers IL-1β, IL-6, IL-8, IL-10, TNFα and IL-12p70 were evaluated. Shapiro-Wilks, Chi-square, ANOVA One-Way and…

Down syndromemedicine.medical_specialtySalivamedicine.medical_treatmentGastroenterologyCerebral palsy03 medical and health sciencesGingivitis0302 clinical medicineStatistical significanceInternal medicinemedicineGeneral Dentistrybusiness.industryResearch030206 dentistrymedicine.disease:CIENCIAS MÉDICAS [UNESCO]Interleukin 10Cytokine030220 oncology & carcinogenesisUNESCO::CIENCIAS MÉDICASOdontostomatology for the Disabled or Special PatientsAnalysis of variancemedicine.symptombusiness
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Innate immunity but not NLRP3 inflammasome activation correlates with severity of stable COPD.

2014

Background In models of COPD, environmental stressors induce innate immune responses, inflammasome activation and inflammation. However, the interaction between these responses and their role in driving pulmonary inflammation in stable COPD is unknown. Objectives To investigate the activation of innate immunity and inflammasome pathways in the bronchial mucosa and bronchoalveolar lavage (BAL) of patients with stable COPD of different severity and control healthy smokers and non-smokers. Methods Innate immune mediators (interleukin (IL)-6, IL-7, IL-10, IL-27, IL-37, thymic stromal lymphopoietin (TSLP), interferon γ and their receptors, STAT1 and pSTAT1) and inflammasome components (NLRP3, NA…

EXPRESSIONMaleINTERLEUKIN-6InflammasomesCOPD PathologyChronic Obstructive Pulmonary DiseaseRespiratory SystemImmunity NLRP3 COPDBronchiReceptors Cell SurfaceRespiratory MucosaPULMONARYInterferon-gammaPulmonary Disease Chronic ObstructiveMARKERSThymic Stromal LymphopoietinSPUTUMNLR Family Pyrin Domain-Containing 3 ProteinCytokine Receptor gp130Humans1506HMGB1 ProteinAdaptor Proteins Signal TransducingAgedScience & TechnologyRECEPTORInterleukinsSmoking1103 Clinical SciencesMiddle AgedInterleukin-1 Receptor-Like 1 ProteinImmunity InnateInnate Immunityrespiratory tract diseasesANTIINFLAMMATORY CYTOKINESTAT1 Transcription FactorCase-Control StudiesT-CELLSASTHMACytokinesFemaleCOPD Pathology Innate ImmunityCarrier ProteinsLife Sciences & BiomedicineBronchoalveolar Lavage FluidSMOKERSThorax
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IL-12 family members in experimental colitis

2008

Interleukin (IL)-12 p35/p40 is a heterodimeric cytokine that plays an important role in T helper (Th) cell polarization and Th1 T-cell differentiation. Recent findings have shown that both p35 and p40 can form other cytokines with different proteins (IL-23: p19/p40; IL-35: p35/EBI3). Furthermore, the cytokine IL-27 (EBI3/p28) has been identified as a member of the IL-12 family. Here, we discuss the recent findings on the role of IL-12 family members in experimental colitis. In particular, the role of IL-23 as a master regulator of effector T-cell activation is highlighted. These findings have important implications for the design of new therapeutic approaches in chronic intestinal inflammat…

EffectorT-Lymphocytesmedicine.medical_treatmentImmunologyInterleukinMaster regulatorExperimental colitishemic and immune systemsEBI3BiologyColitisInflammatory Bowel DiseasesInterleukin-12CytokineIntestinal inflammationImmunologyInterleukin 12medicineAnimalsHumansImmunology and AllergySignal TransductionMucosal Immunology
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IL-6 stimulates annexin 1 expression and translocation and suggests a new biological role as class II acute phase protein.

1998

Annexin 1 (Ax 1), a protein whose synthesis and secretion are induced during the inflammatory response, has been proposed as a mediator of the anti-inflammatory action of glucocorticoids. To gain insight into a broader role of Ax 1 during the inflammatory response, the authors have investigated how pro-inflammatory cytokines [interleukin 1 (IL-1), IL-6 and tumour necrosis factor alpha (TNF-alpha)] affect Ax 1 expression and regulation at transcriptional and translational levels. The authors show that induction of the Ax 1 protein and its translocation to the cell membrane are stimulated by interleukin 6. However neither IL-1 nor TNF-alpha display these effects. Analysis of 5'-deletion mutan…

ElectrophoresisImmunologyAdenocarcinomaBiochemistryDexamethasoneMediatorAnnexinTumor Cells CulturedImmunology and AllergyHumansSecretionRNA MessengerCloning MolecularInterleukin 6Promoter Regions GeneticMolecular BiologyAnnexin A1Reporter genebiologyInterleukin-6Acute-phase proteinInterleukinNuclear ProteinsHematologyMolecular biologyRecombinant ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticMifepristonebiology.proteinCCAAT-Enhancer-Binding ProteinsMutagenesis Site-DirectedTumor necrosis factor alphaAcute-Phase ProteinsTranscription FactorsCytokine
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Hormonal and embryonic regulation of chemokines IL-8, MCP-1 and RANTES in the human endometrium during the window of implantation.

2002

Chemokines are a family of small polypeptides which specialize in the attraction of leukocytes. The presence of specific leukocyte subsets at the implantation site is an important element of the complex, and not completely understood, process of embryonic implantation. This report includes the investigation of the in-vivo immunolocalization and hormonal regulation of interleukin (IL)-8, monocyte chemotactic protein (MCP)-1 and RANTES (regulated upon activation normal T-cell expressed and secreted) in the human endometrium during hormone replacement therapy cycles for oocyte recipients in an IVF programme. In addition, we have analysed the embryonic regulation of these endometrial epithelial…

Embryologymedicine.medical_specialtyChemokineStromal cellmedicine.medical_treatmentFertilization in VitroEndometriumAndrologyEndometriumPregnancyInternal medicineGeneticsmedicineHumansBlastocystInterleukin 8Embryo ImplantationMolecular BiologyChemokine CCL5Chemokine CCL2biologyMonocyteInterleukin-8Obstetrics and GynecologyCell BiologyEmbryonic stem cellCoculture TechniquesEndocrinologymedicine.anatomical_structureCytokineBlastocystReproductive MedicineCulture Media Conditionedbiology.proteinFemaleDevelopmental BiologyMolecular human reproduction
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Apoptosis of oligodendrocytes via Fas and TNF-R1 is a key event in the induction of experimental autoimmune encephalomyelitis.

2005

Abstract In experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, immunization with myelin Ags leads to demyelination and paralysis. To investigate which molecules are crucial for the pathogenesis of EAE, we specifically assessed the roles of the death receptors Fas and TNF-R1. Mice lacking Fas expression in oligodendrocytes (ODCs) were generated and crossed to TNF-R1-deficient mice. To achieve specific deletion of a loxP-flanked fas allele in ODCs, we generated a new insertion transgene, expressing the Cre recombinase specifically in ODCs. Fas inactivation alone as well as the complete absence of TNF-R1 protected mice partially from EAE induced by the imm…

Encephalomyelitis Autoimmune ExperimentalEncephalomyelitisTransgeneT-LymphocytesImmunologyApoptosisMyelin oligodendrocyte glycoproteinMyelinInterferon-gammaMicemedicineImmunology and AllergyAnimalsfas ReceptorReceptorInflammationbiologyMultiple sclerosisExperimental autoimmune encephalomyelitismedicine.diseaseMice Inbred C57BLMyelin-Associated GlycoproteinOligodendrogliamedicine.anatomical_structureApoptosisReceptors Tumor Necrosis Factor Type IImmunologybiology.proteinInterleukin-2Myelin-Oligodendrocyte GlycoproteinMyelin ProteinsDemyelinating DiseasesJournal of immunology (Baltimore, Md. : 1950)
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Smad7 in T cells drives T helper 1 responses in multiple sclerosis and experimental autoimmune encephalomyelitis

2010

Autoreactive CD4+ T lymphocytes play a vital role in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis. Since the discovery of T helper 17 cells, there is an ongoing debate whether T helper 1, T helper 17 or both subtypes of T lymphocytes are important for the initiation of autoimmune neuroinflammation. We examined peripheral blood CD4+ cells from patients with active and stable relapsing-remitting multiple sclerosis, and used mice with conditional deletion or over-expression of the transforming growth factor-beta inhibitor Smad7, to delineate the role of Smad7 in T cell differentiation and autoimmune neuroinflammation. We found that Smad…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisT helper 1Regulatory T cellT cellMolecular Sequence DataMice TransgenicBiologySmad7 ProteinMiceInterleukin 21medicineAnimalsHumansCytotoxic T cellAmino Acid SequenceIL-2 receptorAntigen-presenting cellMice Knockoutintegumentary systemEAEimmune regulationCD28Original ArticlesTh1 CellsNatural killer T cellMice Inbred C57BLmedicine.anatomical_structureT cell responsesImmunologyNeurology (clinical)Brain
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Phosphodiesterase inhibitor pentoxifylline, a selective suppressor of T helper type 1- but not type 2-associated lymphokine production, prevents indu…

1993

The phosphodiesterase inhibitor pentoxifylline (POX), which is known to have pharmacological effects in animal models of multiorgan failure and endotoxin-mediated shock, was tested for its immunosuppressive potential on T lymphocyte activation in vitro and in vivo. POX was found to have a profound inhibitory effect on both mitogen- and antigen-induced proliferation of CD4+ T cells in vitro. This inhibitory activity of the drug could be reproduced by treating T lymphocytes with cAMP analogues during stimulation. Responses of repeatedly in vitro stimulated cells were much more strongly inhibited by the drug and by cAMP analogues than responses of fresh resting lymphocytes. Furthermore, POX co…

Encephalomyelitis Autoimmune ExperimentalPhosphodiesterase InhibitorsEncephalomyelitisT cellImmunologyBiologyLymphocyte ActivationPentoxifyllinemedicineAnimalsImmunology and AllergyPentoxifyllineLymphokinesTumor Necrosis Factor-alphaExperimental autoimmune encephalomyelitisLymphokinevirus diseasesInterleukinT-Lymphocytes Helper-InducerT lymphocytemedicine.diseaseRatsmedicine.anatomical_structureBucladesineRats Inbred LewImmunologyInterleukin-2FemaleTumor necrosis factor alphaInterleukin-4Immunosuppressive Agentsmedicine.drugEuropean Journal of Immunology
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T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma.

2007

T cell functional differentiation is mediated by lineage-specific transcription factors. T helper 17 (Th17) has been recently identified as a distinct Th lineage mediating tissue inflammation. Retinoic acid receptor-related orphan receptor gamma (ROR gamma) was shown to regulate Th17 differentiation; ROR gamma deficiency, however, did not completely abolish Th17 cytokine expression. Here, we report Th17 cells highly expressed another related nuclear receptor, ROR alpha, induced by transforming growth factor-beta and interleukin-6 (IL-6), which is dependent on signal transducer and activator of transcription 3. Overexpression of ROR alpha promoted Th17 differentiation, possibly through the c…

Encephalomyelitis Autoimmune ExperimentalReceptors Retinoic AcidT cellImmunologyRetinoic acidReceptors Cytoplasmic and NuclearElectrophoretic Mobility Shift AssayBiology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineT-Lymphocyte SubsetsmedicineT helper 17 cellImmunology and AllergyAnimalsCell LineageReceptorMOLIMMUNOTranscription factor030304 developmental biologyOrphan receptor0303 health sciencesReceptors Thyroid HormoneReverse Transcriptase Polymerase Chain ReactionInterleukin-17Cell DifferentiationNuclear Receptor Subfamily 1 Group F Member 1T-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3Molecular biologyMice Mutant StrainsCell biologymedicine.anatomical_structureInfectious DiseaseschemistryNuclear receptorSTAT proteinTrans-ActivatorsFemale030215 immunologyImmunity
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Microglial activation milieu controls regulatory T cell responses.

2013

Abstract Although mechanisms leading to brain-specific inflammation and T cell activation have been widely investigated, regulatory mechanisms of local innate immune cells in the brain are only poorly understood. In this study, to our knowledge we show for the first time that MHC class II+CD40dimCD86dimIL-10+ microglia are potent inducers of Ag-specific CD4+Foxp3+ regulatory T cells (Tregs) in vitro. Microglia differentially regulated MHC class II expression, costimulatory molecules, and IL-10 depending on the amount of IFN-γ challenge and Ag dose, promoting either effector T cell or Treg induction. Microglia-induced Tregs were functionally active in vitro by inhibiting Ag-specific prolifer…

Encephalomyelitis Autoimmune ExperimentalRegulatory T cellT cellImmunologychemical and pharmacologic phenomenaMice TransgenicLymphocyte ActivationT-Lymphocytes RegulatoryImmune toleranceInterferon-gammaMiceImmune systemT-Lymphocyte SubsetsmedicineImmune ToleranceImmunology and AllergyAnimalsCells CulturedCD86MHC class IIbiologyMicrogliaHistocompatibility Antigens Class IIFOXP3Brainhemic and immune systemsForkhead Transcription FactorsCoculture TechniquesCell biologyInterleukin-10Mice Inbred C57BLmedicine.anatomical_structureCellular Microenvironmentbiology.proteinMicrogliaJournal of immunology (Baltimore, Md. : 1950)
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