Search results for " IL-2"

showing 10 items of 12 documents

IL-17 polarization of MAIT cells is derived from the activation of two different pathways

2017

MAIT cells are expanded in salivary glands of patients with Sjogren's syndrome and are IL-17 polarized. IL-7 and IL-23 induce IL-17 production activating two different pathways: IL-7 stimulation induces in fact a significant STAT3 and HIF1alpha upregulation, conversely, IL-23 stimulation significantly induces RORc overexpression in MAIT cells of patients with Sjogren's syndrome.

0301 basic medicineImmunologyStimulationInterleukin-23Mucosal-Associated Invariant T CellsSalivary GlandsSTAT303 medical and health sciencesIL-17; IL-23; IL-7; MAIT cells; RORc; Sjogren's Syndrome; STAT3; Immunology and Allergy; Immunology0302 clinical medicinestomatognathic systemDownregulation and upregulationRAR-related orphan receptor gammaIL-23Interleukin 23HumansImmunology and AllergySTAT3MAIT cellIL-7biologyInterleukin-17MAIT CellsCell biologyRORcIL-17Settore MED/16 - Reumatologia030104 developmental biologySjogren's Syndromebiology.proteinInterleukin 17030215 immunology
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Intestinal dysbiosis and innate immune responses in axial spondyloarthritis

2016

Purpose of review Inflammatory innate and adaptive immune cell responses to commensal bacteria underlie the pathogenesis of human chronic inflammatory diseases. Intestinal dysbiosis has been described in patients with spondyloarthritis (SpA) and seems to be correlated with histologic and immunologic alterations. Purpose of this review is to discuss the relationship occurring between intestinal dysbiosis and innate immune responses in patients with axial SpA. Recent findings Intestinal dysbiosis and differential activation of intestinal immune responses in patients with SpA have been demonstrated. Furthermore, innate cells that appear to be involved in the pathogenesis of SpA may control int…

0301 basic medicinePathogenesis03 medical and health sciences0302 clinical medicineImmune systemRheumatologyImmunityIL-23dysbiosis; gut inflammation; IL-17; IL-23; IL-9; innate lymphoid cells; spondyloarthritis; RheumatologySpondylarthritisInterleukin 23MedicineHumansspondyloarthriti030203 arthritis & rheumatologyInnate immune systemBacteriabusiness.industrydysbiosiInnate lymphoid cellmedicine.diseaseIL-9Immunity InnateGastrointestinal MicrobiomeIntestinesIL-17030104 developmental biologyImmunologyinnate lymphoid cellDysbiosisInterleukin 17gut inflammationbusinessDysbiosis
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IL-25 dampens the growth of human germinal center-derived B-cell non Hodgkin Lymphoma by curtailing neoangiogenesis

2018

Interleukin (IL)-25, a member of the IL-17 cytokine superfamily, is produced by immune and non-immune cells and exerts type 2 pro-inflammatory effects in vitro and in vivo. The IL-25 receptor(R) is composed of the IL-17RA/IL-17RB subunits. Previous work showed that germinal centre (GC)-derived B-cell non Hodgkin lymphomas (B-NHL) expressed IL-17AR, formed by IL-17RA and IL-17RC subunits, and IL-17A/IL-17AR axis promoted B-NHL growth by stimulating neoangiogenesis. Here, we have investigated expression and function of IL-25/IL-25R axis in lymph nodes from human GC-derived B-NHL, i.e. Follicular Lymphoma (FL,10 cases), Diffuse Large B Cell Lymphoma (6 cases) and Burkitt Lymphoma (3 cases). Tu…

0301 basic medicinelcsh:Immunologic diseases. AllergyPathologymedicine.medical_specialtyAngiogenesismedicine.medical_treatmentImmunologyFollicular lymphomalcsh:RC254-282Angiogenesis; B lymphocytes; B-NHL; Cytokines; IL-25; Tumor immunology; Immunology and Allergy; Immunology; Oncology03 medical and health sciencesangiogenesisIL-25immune system diseaseshemic and lymphatic diseasesmedicineImmunology and AllergyCytokineOriginal ResearchB lymphocyteChemistryGerminal centerInterleukinmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenscytokinesLymphomaAngiogenesi030104 developmental biologyCytokineOncologyCancer researchB-Cell Non-Hodgkin LymphomaTumor immunologyB-NHLb lymphocyteslcsh:RC581-607Diffuse large B-cell lymphoma
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IL-21 regulates experimental colitis by modulating the balance between Treg and Th17 cells

2007

Regulatory T (T(reg)) cells play a key role in the maintenance of the immune system homeostasis. T(reg) cells can be generated in the periphery under control of TGF-beta, a cytokine involved in the negative control of the immune system. However, TGF-beta cooperates with IL-6 in the generation of Th17 cells, a novel class of effector cells involved in numerous inflammatory diseases, including colitis. Therefore, TGF-beta emerges as a mediator of both anti-inflammatory and pro-inflammatory processes, depending on the local cytokine milieu. Here we demonstrate that IL-21, a type-1 cytokine produced by T cells and involved in the pathogenesis of immune-mediated diseases, prevents the TGF-beta-d…

Adoptive cell transfermedicine.medical_treatmentImmunologyCellGene Expressionchemical and pharmacologic phenomenaMice SCIDBiologyT-Lymphocytes RegulatoryMiceImmune systemT-Lymphocyte SubsetsTransforming Growth Factor betaFoxP3IL-21medicineAnimalsImmunology and AllergyRNA MessengerIL-2 receptorTranscription factorSettore MED/12 - GastroenterologiaMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionInterleukinsInterleukin-17FOXP3Forkhead Transcription Factorshemic and immune systemsColitisFlow CytometryAdoptive TransferCell biologyColitis; FoxP3; IL-21; Treg cells; TGF-βTGF-βDisease Models Animalmedicine.anatomical_structureCytokineImmunologyTreg cellsHomeostasisEuropean Journal of Immunology
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Potential involvement of IL-22 and IL-22-producing cells in the inflamed salivary glands of patients with Sjogren's syndrome.

2012

OBJECTIVES: In chronic inflammatory disorders, interleukin (IL)-22 may act either as a protective or as a pro-inflammatory cytokine. At mucosal sites, IL-22 is mainly produced by CD4(+) T cells and by a subset of mucosal natural killer (NK) cells expressing the receptor NKp44 (NKp44(+) NK cells). The aim of this study was to investigate the IL-22 expression in the salivary glands of patients with primary Sjögren's syndrome (pSS). METHODS: Minor salivary gland biopsies were obtained from 19 patients with pSS and 16 with non-specific chronic sialoadenitis. Quantitative gene expression analysis by TaqMan real-time PCR and immunohistochemistry for IL-17, IL-22, IL-23 and STAT3 (signal transduce…

AdultCD4-Positive T-LymphocytesMaleSTAT3 Transcription FactorAnkylosing Spondylitis IL-22 NKp44NK cells intestinal inflammationmedicine.medical_treatmentImmunologySalivary Glands MinorInterleukin-23General Biochemistry Genetics and Molecular BiologySialadenitisInterleukin 22PathogenesisRheumatologyintestinal inflammationIL-22Immunology and AllergyMedicineHumansRNA MessengerSTAT3ReceptorAgedAnkylosing SpondylitibiologySalivary glandNatural Cytotoxicity Triggering Receptor 2business.industryReverse Transcriptase Polymerase Chain ReactionInterleukinsInterleukin-17InterleukinMiddle AgedNKp44NK cellKiller Cells NaturalSettore MED/16 - ReumatologiaCytokinemedicine.anatomical_structureSjogren's SyndromeCase-Control StudiesImmunologybiology.proteinImmunohistochemistryFemalebusinessAnnals of the rheumatic diseases
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Interleukin-22 and interleukin-22-producing NKp44+ natural killer cells in subclinical gut inflammation in ankylosing spondylitis

2012

Objective The intestinal inflammation observed in patients with ankylosing spondylitis (AS) is characterized by an overexpression of interleukin-23 (IL-23). IL-23 is known to regulate IL-22 production through lamina propria NKp44+ natural killer (NK) cells, which are thought to be involved in protective mucosal mechanisms. This study was undertaken to evaluate the frequency of NKp44+ NK cells and the expression of IL-22 in the ileum of AS patients. Methods Tissue NKp44+ NK cells, NKp46+ NK cells, and IL-22–producing cells were analyzed by flow cytometry. Quantitative gene expression analysis of IL-22, IL-23, IL-17, STAT-3, and mucin 1 (MUC-1) was performed by reverse transcriptase–polymeras…

AdultMaleSTAT3 Transcription FactorImmunologyIleumBiologyInterleukin-23Peripheral blood mononuclear cellFlow cytometryAnkylosing spondylitis IL-22 intestinal inflammation intestinal inflammationInterleukin 22Interleukin 21RheumatologyIleumintestinal inflammationIL-22medicineHumansImmunology and AllergySpondylitis AnkylosingPharmacology (medical)Intestinal MucosaInflammationLamina propriaNatural Cytotoxicity Triggering Receptor 2medicine.diagnostic_testInterleukinsMucin-1MucinMiddle AgedKiller Cells NaturalAnkylosing spondylitimedicine.anatomical_structureImmunologyImmunohistochemistryFemaleArthritis & Rheumatism
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Data mining-based statistical analysis of biological data uncovers hidden significance: clustering Hashimoto’s thyroiditis patients based on the resp…

2014

The pathogenesis of Hashimoto's thyroiditis includes autoimmunity involving thyroid antigens, autoantibodies, and possibly cytokines. It is unclear what role plays Hsp60, but our recent data indicate that it may contribute to pathogenesis as an autoantigen. Its role in the induction of cytokine production, pro- or anti-inflammatory, was not elucidated, except that we found that peripheral blood mononucleated cells (PBMC) from patients or from healthy controls did not respond with cytokine production upon stimulation by Hsp60 in vitro with patterns that would differentiate patients from controls with statistical significance. This "negative” outcome appeared when the data were pooled and ana…

Interleukin 2Hashimoto’s thyroiditiShort Communicationmedicine.medical_treatmentStimulationHashimoto Diseasecomputer.software_genremedicine.disease_causeBiochemistryClusteringThyroiditisAutoimmunityInterferon-gammaCluster AnalysisData MiningHumansMedicineHashimoto DiseaseDelta valueIFN-γCells CulturedSettore BIO/16 - Anatomia Umanabusiness.industryIL-2ThyroidChaperonin 60Cell BiologyHsp60medicine.diseasemedicine.anatomical_structureCytokineClustering; Data mining; Delta values; Hashimoto’s thyroiditis; Hsp60; IFN-γ; IL-2ImmunologyLeukocytes MononuclearInterleukin-2Biomarker (medicine)Data miningbusinesscomputerAlgorithmsmedicine.drug
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Molecular basis of burn wound healing in diabetics: the effect of vitamin B17, metformin, and autologous fat stem cells

Keywords: Diabetes wound healing amygdaline (vitamin B17) inflammation Metformin adipose tissue stem cells IL-2 IL-6 IL-10 and HSP-70.
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Role of IL-28B and inosine triphosphatase polymorphisms in efficacy and safety of Peg-Interferon and ribavirin in chronic hepatitis C compensated cir…

2013

Genetic factors can influence the outcome of antiviral therapy in chronic hepatitis C (HCV). We evaluated the role of interleukin-28B single nucleotide polymorphisms (SNPs) and inosine triphosphatase (ITPA) gene variants in HCV cirrhosis treated with Peg-Interferon and ribavirin. A prospective cohort of 233 patients with compensated cirrhosis received 1-1.5 μg/kg/week of Peg-Interferon alpha-2b plus 1000-1200 mg/day of RBV for 48 weeks. A sustained virologic response (SVR) was achieved in 27% of patients. On multivariate logistic analysis, the absence of oesophageal varices (OR 3.64 CI 95% 1.27-10.44 P = 0.016), infection with genotype 2 or 3 (OR 4.06, CI 95% 1.08-15.26, P = 0.038), C/C all…

Liver CirrhosisMaleSettore MED/07 - Microbiologia E Microbiologia ClinicaAnemia HemolyticGenotypeHepacivirusInterferon alpha-2Esophageal and Gastric VaricesAntiviral AgentsPolymorphism Single NucleotidePolyethylene GlycolsSettore BIO/13 - Biologia ApplicataRibavirinHumanschronic hepatitis C cirrhosis IL-28B inosine triphosphatase sustained virologic responseProspective StudiesPyrophosphatasesGenetic Association StudiesAgedSettore MED/12 - GastroenterologiaDose-Response Relationship DrugInterleukinsInterferon-alphaSequence Analysis DNAHepatitis C ChronicMiddle AgedRecombinant ProteinsLogistic ModelsTreatment OutcomeMultivariate AnalysisDrug Therapy CombinationFemaleInterferonsJournal of viral hepatitis
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Interleukin (IL)-22 receptor 1 is over-expressed in primary Sjogren's syndrome and Sjögren-associated non-Hodgkin lymphomas and is regulated by IL-18.

2015

Summary The aim of this study was to elucidate more clearly the role of interleukin (IL)-18 in modulating the IL-22 pathway in primary Sjögren's syndrome (pSS) patients and in pSS-associated lymphomas. Minor salivary glands (MSGs) from patients with pSS and non-specific chronic sialoadenitis (nSCS), parotid glands biopsies from non-Hodgkin lymphomas (NHL) developed in pSS patients, were evaluated for IL-18, IL-22, IL-22 receptor 1 (IL-22R1), IL-22 binding protein (IL-22BP) and signal transducer and activator of transcription-3 (STAT-3) expression. MSGs IL-22R1-expressing cells were characterized by confocal microscopy and flow cytometry in pSS, nSCS and healthy controls. The effect of recom…

MaleSalivary Glandslaw.inventionInterleukin 22lawIL-22Immunology and AllergyMyeloid CellsIL-22R1Receptormedicine.diagnostic_testnon-Hodgkin lymphomaLymphoma Non-HodgkinInterleukin-17TranslationalInterleukin-18Lacrimal ApparatusInterleukinMiddle AgedHaematopoiesisSjogren's SyndromeIL-22BPRecombinant DNASjögren's syndromeInterleukin 18FemaleIL-18Signal TransductionAdultSTAT3 Transcription FactorImmunologyPrimary Cell CultureBiologyPeripheral blood mononuclear cellIL-18; IL-22; IL-22BP; IL-22R1; Sjögren's syndrome; non-Hodgkin lymphomaSialadenitisFlow cytometrystomatognathic systemmedicineHumansAgedInterleukinsMacrophagesReceptors InterleukinSettore MED/16 - Reumatologiastomatognathic diseasesGene Expression RegulationImmunologyLeukocytes MononuclearClinical and experimental immunology
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