Search results for "Interleukin 2"

showing 10 items of 320 documents

IL28B and PNPLA3 Polymorphisms Affect Histological Liver Damage in Patients with Non-alcoholic Fatty Liver Disease.

2012

Background & Aims: Genetic background may affect liver damage in patients with non-alcoholic fatty liver disease (NAFLD). The main outcomes of the study were to assess whether IL28B rs12979860 and rs8099917 polymorphisms, together with PNPLA3 rs738409 C>G polymorphism, are associated with lobular inflammation and fibrosis, in NAFLD patients. Methods: One hundred sixty consecutive NAFLD patients were assessed by liver biopsy (Kleiner score); anthropometric, and biochemical and metabolic features were included. IL28B rs12979860 C>T, IL28B rs8099917 G>C, and PNPLA3 rs738409 C>G single nucleotide polymorphisms were tested. Results: Seventy-four (46.2%) patients had IL28B rs12979860 CC polymorph…

Univariate analysismedicine.medical_specialtyPathologySettore MED/12 - GastroenterologiaHepatologymedicine.diagnostic_testFatty liverliver fibrosiSingle-nucleotide polymorphismBiologySettore MED/08 - Anatomia Patologicamedicine.diseaseGastroenterologynonalcoholic fatty liver IL28B PNPLA3 PolymorphismsInterleukin 28BFibrosisInternal medicineLiver biopsyGenotypemedicinenafld liver biopsyHyperuricemia
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Smad7 controls resistance of colitogenic T cells to regulatory T cell-mediated suppression.

2008

Background & Aims Foxp3-expressing regulatory T cells (Tregs) play a key role in the maintenance of the gut immune homeostasis, and an intact transforming growth factor (TGF)-β signaling is required for their function. In inflammatory bowel disease (IBD), the TGF-β signaling is impaired because of high expression of the inhibitory molecule Smad7. Although no intrinsic defects in Tregs function have been shown in IBD, it is still unknown whether colitogenic T cells are susceptible to Treg-mediated suppression. In this study, we have investigated whether IBD mucosal CD4+ T cells are resistant to Tregs and whether Smad7 is involved in this process. Methods IBD lamina propria mononuclear cells …

antisense oligonucleotideCD4-Positive T-LymphocytesAdoptive cell transferT-Lymphocytesanimal cellCell CommunicationInbred C57BLT-Lymphocytes RegulatoryTransgenicMiceregulatory T lymphocyteCrohn DiseaseTransforming Growth Factor betamononuclear cellRAG1 proteinIntestinal MucosaenteritisCells CulturedMice KnockoutSettore MED/12 - GastroenterologiaCulturedintegumentary systemmedicine.diagnostic_testarticleGastroenterologyInterleukinhemic and immune systemsT helper cellColitisRegulatoryUp-Regulationmedicine.anatomical_structurepriority journalgamma interferonSignal TransductionRegulatory T cellColonCellsKnockoutanimal experimentinterleukin 6chemical and pharmacologic phenomenaMice TransgenicBiologyinterleukin 2Recombination-activating geneFlow cytometryProinflammatory cytokineSmad7 ProteinmedicineAnimalsHumanscontrolled studyhumanlamina propriamouseCell ProliferationHomeodomain ProteinsCD4+ T lymphocytenonhumanHepatologyAnimalflow cytometryhuman cellanimal cell culturetransgenic mouseMice Inbred C57BLDisease Models Animalantisense oligonucleotide; gamma interferon; interleukin 17; interleukin 2; interleukin 6; RAG1 protein; Smad7 protein; animal cell; animal cell culture; animal experiment; article; CD4+ T lymphocyte; cell proliferation; colitis; controlled study; enteritis; flow cytometry; human; human cell; knockout mouse; lamina propria; mononuclear cell; mouse; nonhuman; priority journal; regulatory T lymphocyte; transgenic mouse; Animals; CD4-Positive T-Lymphocytes; Cell Communication; Cell Proliferation; Cells Cultured; Colitis; Colon; Crohn Disease; Disease Models Animal; Homeodomain Proteins; Humans; Intestinal Mucosa; Mice; Mice Inbred C57BL; Mice Knockout; Mice Transgenic; Signal Transduction; Smad7 Protein; T-Lymphocytes Regulatory; Transforming Growth Factor beta; Up-RegulationDisease ModelsImmunologyinterleukin 17knockout mouseTransforming growth factorGastroenterology
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Rituximab modulates the expression of IL-22 in the salivary glands of patients with primary Sjogren's syndrome

2012

We have recently demonstrated that interleukin (IL)-22, mainly produced by T-helper 17 effector cells, natural killer (NK)p44+NK cells and epithelial cells, may be potentially involved in the pathogenesis of primary Sjogren's syndrome (pSS).1 The IL-22/IL-22R pathway is known to play a role in the emergence of T and B-cell lymphoma2 ,3 and pSS is considered a risk factor for the development of lymphoma.4 Rituximab, which has historically been used for the treatment of B-cell lymphoma,5 has also been considered to be effective in the therapy of pSS.6 Ten consecutive patients with pSS (eight women and two men, with a mean duration of disease of 48±18 months), diagnosed according to the Americ…

biologybusiness.industryImmunologyInterleukinmedicine.diseaseGeneral Biochemistry Genetics and Molecular BiologyLymphomaInterleukin 22Pathogenesissjogren's syndromestomatognathic diseasesRituximab sjogren's syndromeRheumatologyMonoclonalImmunologymedicinebiology.proteinImmunology and AllergyRituximabAntibodyRisk factorbusinessRituximabmedicine.drug
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ID: 213

2015

The epithelium is the main entry point for many viruses, but the processes that protect barrier surfaces against viral infections are incompletely understood. Here we identified interleukin 22 (IL-22) produced by innate lymphoid cell group 3 (ILC3) as an amplifier of signaling via interferon- λ (IFN- λ ) , a synergism needed to curtail the replication of rotavirus, the leading cause of childhood gastroenteritis. Cooperation between the receptor for IL-22 and the receptor for IFN- λ , both of which were ‘preferentially’ expressed by intestinal epithelial cells (IECs), was required for optimal activation of the transcription factor STAT1 and expression of interferon-stimulated genes (ISGs). T…

biologymedicine.medical_treatmentImmunologyInnate lymphoid cellHematologyImmunotherapymedicine.disease_causeBiochemistryVirologyInterleukin 22Viral replicationInterferonRotavirusImmunologymedicinebiology.proteinImmunology and AllergySTAT1Molecular BiologyTranscription factormedicine.drugCytokine
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OP0081 Aberrant Expression of IL-22RA1 on Hematopoietic Cells as Immunologically Signature of Primary Sjogren’s Syndrome and Sjogren-Associated Non-H…

2013

Background Interleukin (IL)-22 is a potent mediator of cellular inflammatory responses that has been recently reported to play a role in the pathogenesis of primary Sjogren’s Syndrome (p-SS) (1, 2) and of T and B lymphomas. IL-22 biological activity is initiated by binding to a cell-surface complex composed of two subunits, IL-22R1 and IL-10R2 receptor chains, and further regulated by interactions with a soluble binding protein, IL-22BP. Unlike the IL-10R2, which is constitutively expressed in many human tissues, IL-22R1 is not detectable in immune cells. Objectives Aim of this study was to better characterize the role of IL-22 axis in the pathogenesis of p-SS and p-SS-associated lymphomas.…

business.industryCD68ImmunologyInterleukinmedicine.diseasePeripheral blood mononuclear cellGeneral Biochemistry Genetics and Molecular BiologyLymphomaInterleukin 22PathogenesisHaematopoiesisImmune systemRheumatologyImmunologyCancer researchImmunology and AllergyMedicinebusinessAnnals of the Rheumatic Diseases
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Ultraviolet B light attenuates the systemic immune response in central nervous system autoimmunity

2014

Objective: Environmental conditions (eg, latitude) play a critical role in the susceptibility and severity of many autoimmune disorders, including multiple sclerosis (MS). Here, we investigated the mechanisms underlying the beneficial effects of immune regulatory processes induced in the skin by moderate ultraviolet B (UVB) radiation on central nervous system (CNS) autoimmunity. Methods: Effects of UVB light were analyzed in a murine model of CNS autoimmunity (experimental autoimmune encephalomyelitis). Additionally, patients with relapsing–remitting MS were treated with narrowband UVB phototherapy. Immunomodulatory effects were examined in skin biopsies, serum samples, and immune cells of …

integumentary systemmedicine.medical_treatmentExperimental autoimmune encephalomyelitischemical and pharmacologic phenomenaInflammationBiologymedicine.disease_causemedicine.diseaseAutoimmunityImmune toleranceInterleukin 21Immune systemCytokineNeurologyImmunityImmunologymedicineNeurology (clinical)medicine.symptomAnnals of Neurology
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RUNX3 and T-Bet in Immunopathogenesis of Ankylosing Spondylitis—Novel Targets for Therapy?

2019

Susceptibility to ankylosing spondylitis (AS) is polygenic with more than 100 genes identified to date. These include HLA-B27 and the aminopeptidases (ERAP1, ERAP2, and LNPEPS), which are involved in antigen processing and presentation to T-cells, and several genes (IL23R, IL6R, STAT3, JAK2, IL1R1/2, IL12B, and IL7R) involved in IL23 driven pathways of inflammation. AS is also strongly associated with polymorphisms in two transcription factors, RUNX3 and T-bet (encoded by TBX21), which are important in T-cell development and function. The influence of these genes on the pathogenesis of AS and their potential for identifying drug targets is discussed here.

lcsh:Immunologic diseases. Allergy0301 basic medicineTBX21Mini ReviewImmunologyBiologyCD8-Positive T-Lymphocytesmedicine.disease_causeAminopeptidasesInterleukin-23Polymorphism Single NucleotideAutoimmunity03 medical and health sciences0302 clinical medicineankylosing spondylitisInterleukin 23medicineImmunology and AllergyHumansImmunologic FactorsSpondylitis AnkylosingMolecular Targeted TherapyInterleukin-7 receptorTranscription factorHLA-B27 AntigenAnkylosing spondylitistherapyAntigen processingautoimmunityReceptors Interleukinmedicine.disease3. Good healthKiller Cells Natural030104 developmental biologyCore Binding Factor Alpha 3 SubunitGene Expression RegulationinflammationImmunologylcsh:RC581-607T-Box Domain ProteinsFunctional genomicsfunctional genomics030215 immunologyFrontiers in Immunology
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Role of the IL-23/IL-17 Pathway in Rheumatic Diseases: An Overview

2021

Interleukin-23 (IL-23) is a pro-inflammatory cytokine composed of two subunits, IL-23A (p19) and IL-12/23B (p40), the latter shared with Interleukin-12 (IL-12). IL-23 is mainly produced by macrophages and dendritic cells, in response to exogenous or endogenous signals, and drives the differentiation and activation of T helper 17 (Th17) cells with subsequent production of IL-17A, IL-17F, IL-6, IL-22, and tumor necrosis factor α (TNF-α). Although IL-23 plays a pivotal role in the protective immune response to bacterial and fungal infections, its dysregulation has been shown to exacerbate chronic immune-mediated inflammation. Well-established experimental data support the concept that IL-23/IL…

lcsh:Immunologic diseases. Allergy0301 basic medicinemedicine.medical_treatmentImmunologyinflammatory diseasesInflammationautoimmune diseaseAutoimmunityReviewInflammatory bowel diseaseInterleukin-23Th17 CellRheumatic Disease03 medical and health sciencesPsoriatic arthritis0302 clinical medicineImmune systemIL-23PsoriasisRheumatic DiseasesInterleukin 23medicineAnimalsHumansImmunology and Allergyautoimmune diseasesMolecular Targeted TherapyIL-23/IL-17 axi030203 arthritis & rheumatologyInflammationbusiness.industryIL-23/IL-17 axisAnimalInterleukin-17medicine.diseaseinflammatory diseaseIL-17030104 developmental biologyCytokineImmunologyTh17 CellsInterleukin 17medicine.symptomlcsh:RC581-607businessHuman
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A10.18 Lack of Association of Serum Interleukin-17 and Interleukin-23 Levels with Disease Activity in Patients with Ankylosing Spondylitis in Latvia

2013

Background Ankylosing spondylitis (AS) is a clinically well-known chronic inflammatory disease of the axial skeleton and peripheral joints. The pathogenesis of this disease still remains a challenge. Determination of cytokine profile and its role involved in AS pathogenesis give an opportunity to extend the targeted therapeutic approach. Interleukin-17 (IL-17) and interleukin-23 (IL-23) are cytokines of interest in the investigation of the pathogenesis of spondyloarthritides although their importance in AS is not clearly defined. Objectives to investigate levels of IL-17 and IL-23 in a group of AS and in a demographically matched group of healthy subjects and its association with the diseas…

medicine.medical_specialtyAnkylosing spondylitismedicine.diagnostic_testbusiness.industryImmunologyInflammationDiseasemedicine.diseaseGastroenterologyGeneral Biochemistry Genetics and Molecular BiologyPathogenesisRheumatologyInternal medicineErythrocyte sedimentation rateImmunologyInterleukin 23Immunology and AllergyMedicineInterleukin 17medicine.symptombusinessBASDAIAnnals of the Rheumatic Diseases
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The role of innate and lymphoid IL-22-producing cells in the immunopathology of primary Sjögren's syndrome

2014

In primary Sjögren's syndrome (pSS) a complex of interconnections between epithelial barrier, innate and adaptive immunity occurs. IL-22 is a pleiotropic cytokine that in pSS may be placed at the intersection of the adaptive and innate branches of immunity. Some evidence suggests that, in pSS, IL-22 may play a prominent pro-inflammatory role driving the early phase of tissue and systemic inflammation and participating in the self-perpetuation of disease. Despite contradictory data in literature about the role of NK cells in pSS, recent data also suggest an important contribution of this subset of cells of the innate immune system in the development and perpetuation of inflammation. Here, we…

musculoskeletal diseasesImmunologyInflammationAdaptive ImmunitySystemic inflammationInterleukin 22stomatognathic systemImmunityImmunopathologymedicineHumansImmunology and AllergyInnateKiller CellInnate immune systembusiness.industryInterleukinsInnate lymphoid cellImmunityInterleukinAcquired immune systemeye diseasesImmunity InnateKiller Cells Naturalstomatognathic diseasesSjogren's SyndromeImmunologyNaturalmedicine.symptombusinessHuman
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