Search results for "Pathogenesis"

showing 10 items of 761 documents

Update on the role of molecular factors and fibroblasts in the pathogenesis of Dupuytren’s disease

2016

The mechanism by which the fibroblast is able to trigger palmar fibromatosis is still not yet fully understood. It would appear certain that the “abnormal” fibroblasts continuously synthesise profibrotic cytokines which are able to determine the activation to myofibroblasts, to stimulate them to the further proliferation and synthesis of other cytokines, to modify the cells’ differentiation and ultrastructural characteristics, as well as the production of matrix and other proteins. Several fibroblast growth factors have been suggested to be responsible of an abnormal cell activation with an aberrantly elevated collagen synthesis and extracellular deposition in Dupuytren’s disease, as TGF-Be…

0301 basic medicinemedicine.medical_specialtySettore MED/19 - Chirurgia PlasticaReviewMatrix metalloproteinaseFibroblast growth factorBiochemistryPathogenesis03 medical and health sciences0302 clinical medicineInternal medicinemedicineExtracellularFibroblastMolecular BiologyCytokines Fibroblast Dupuytren’s disease030222 orthopedicsbiologyCell Biology030104 developmental biologyEndocrinologymedicine.anatomical_structurebiology.proteinCancer researchMyofibroblastPlatelet-derived growth factor receptorPalmar Fibromatosis
researchProduct

Possible Roles of IL-33 in the Innate-Adaptive Immune Crosstalk of Psoriasis Pathogenesis

2019

Background. IL-33 belongs to the IL-1 family, playing a role in several biologic processes as well as in the pathogenesis of different diseases, including skin pathologies. It acts as an alarmin, released by damaged cells. Binding to a ST2 receptor, it stimulates many immune cells such as ILC2 and Th2 cells. IL-33/ST2 axis seems to be involved in Th17 response. According to this, a review was performed to analyze if IL-33 even interplay in the onset of psoriasis, a Th1/Th17 inflammatory disease. Methods. Data obtained from the included articles are study author name, publication date, group studied, clinical and biological variables, laboratory tests, and outcome of interest of the study. R…

0301 basic medicinemedicine.medical_treatmentImmunologyDiseaseReview ArticlePathogenesis03 medical and health sciencesPsoriatic arthritis0302 clinical medicineImmune systemPsoriasismedicinelcsh:PathologyHumansPsoriasisbusiness.industryCell BiologyTh1 Cellsmedicine.diseaseInterleukin-33Immunity InnateInterleukin 33030104 developmental biologyCytokine030220 oncology & carcinogenesisImmunologyTh17 CellsTumor necrosis factor alphabusinesslcsh:RB1-214Mediators of Inflammation
researchProduct

Autoantibodies in Spondyloarthritis, Focusing on Anti-CD74 Antibodies

2019

Spondyloarthritis (SpA) is an inflammatory rheumatic disease with diverse clinical presentation. The diagnosis of SpA remains a big challenge in daily clinical practice because of the limitation in specific biomarkers of SpA, more biomarkers are still needed for SpA diagnosis and disease activity monitoring. In the past, SpA was considered predominantly as auto-inflammatory disease vs. autoimmune disease. However, in recent years several researches demonstrated a broad autoantibody response in SpA patients. Study also indicated that mice lack of ZAP70 in T cell develop SpA featured inflammation. These studies indicated the autoimmune features of SpA and gave rise to the potential use of aut…

0301 basic medicinemusculoskeletal diseaseslcsh:Immunologic diseases. AllergyCD74autoantibodiesdiagnosisImmunologyAutoimmunityDiseaseAutoantigensAutoimmune DiseasesPathogenesis03 medical and health sciences0302 clinical medicineHypothesis and TheorySpondylarthritismedicineImmunology and AllergyHumansHeat-Shock ProteinsAutoimmune diseasebiologybusiness.industryChinese patientsAutoantibodyHistocompatibility Antigens Class IIspondyloarthritismedicine.diseaseClinical PracticeAntigens Differentiation B-LymphocyteProtein Phosphatase 2Cstomatognathic diseases030104 developmental biology14-3-3 ProteinsROC CurveImmunologybiology.proteinBiomarker (medicine)Antibodybusinessbeta 2-Microglobulinlcsh:RC581-607Biomarkers030215 immunologyanti-CD74 autoantibodyFrontiers in Immunology
researchProduct

HSP60 activity on human bronchial epithelial cells

2017

HSP60 has been implicated in chronic inflammatory disease pathogenesis, including chronic obstructive pulmonary disease (COPD), but the mechanisms by which this chaperonin would act are poorly understood. A number of studies suggest a role for extracellular HSP60, since it can be secreted from cells and bind Toll-like receptors; however, the effects of this stimulation have never been extensively studied. We investigated the effects (pro- or anti-inflammatory) of HSP60 in human bronchial epithelial cells (16-HBE) alone and in comparison with oxidative, inflammatory, or bacterial challenges. 16-HBE cells were cultured for 1–4 h in the absence or presence of HSP60, H2O2, lipopolysaccharide (…

0301 basic medicinep38αSettore BIO/17 - IstologiaLipopolysaccharidep38 mitogen-activated protein kinasesImmunologyStimulationBronchip38 Mitogen-Activated Protein KinasesERK1Cell LinePathogenesisMitochondrial Proteins03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOriginal Research ArticlesHumansImmunology and AllergyCOPDInterleukin 8Protein kinase AReceptor16-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; TLR-4; p38αPharmacologyIL-8Settore BIO/16 - Anatomia UmanaInterleukin-8JNK1NF-κB p65 subunitEpithelial CellsTLR-4Chaperonin 60MyD88Interleukin-1016-HBEToll-Like Receptor 416-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; p38α; TLR-4; Immunology and Allergy; Immunology; PharmacologyInterleukin 10030104 developmental biologychemistry030220 oncology & carcinogenesisIL-10Cancer researchCREB1NF-κB p65 subunitHSP60p38α
researchProduct

The MID1 protein is a central player during development and in disease.

2015

Loss-of-function mutations in the MID1 gene cause a rare monogenic disorder, Opitz BBB/G syndrome (OS), which is characterized by malformations of the ventral midline. The MID1 gene encodes the MID1 protein, which assembles a large microtubule-associated protein complex. Intensive research over the past several years has shed light on the function of the MID1 protein as a ubiquitin ligase and regulator of mTOR signalling and translational activator. As a central player in the cell MID1 has been implicated in the pathogenesis of various other disorders in addition to OS including cancer and neurodegenerative diseases. Influencing the activity of the MID1 protein complex is a promising new st…

0301 basic medicinephysiopathology [Huntington Disease]CarcinogenesisUbiquitin-Protein LigasesRegulatorDiseaseBiologyBioinformaticsmedicine.disease_causephysiopathology [Alzheimer Disease]Congenital AbnormalitiesPathogenesis03 medical and health sciencesMiceAlzheimer Diseasephysiology [Nuclear Proteins]medicineAnimalsHumansgenetics [Microtubule Proteins]ddc:610GenePI3K/AKT/mTOR pathwayActivator (genetics)Nuclear Proteinsgenetics [Nuclear Proteins]genetics [Transcription Factors]physiology [Transcription Factors]Ubiquitin ligase030104 developmental biologyHuntington DiseaseMutationbiology.proteinMicrotubule Proteinsphysiology [Microtubule Proteins]CarcinogenesisMid1 protein humanTranscription FactorsFrontiers in bioscience (Landmark edition)
researchProduct

PNPLA3 and TLL-1 Polymorphisms as Potential Predictors of Disease Severity in Patients With COVID-19

2021

Albeit the pathogenesis of COVID-19 remains unclear, host’s genetic polymorphisms in genes involved in infection and reinfection, inflammation, or immune stimulation could play a role in determining the course and outcome. We studied in the early phase of pandemic consecutive patients (N = 383) with SARS-CoV-2 infection, whose subsequent clinical course was classified as mild or severe, the latter being characterized by admission to intensive therapy unit or death. Five host gene polymorphisms (MERTK rs4374383, PNPLA3 rs738409, TLL-1 rs17047200, IFNL3 rs1297860, and INFL4 rs368234815) were assessed by using whole nucleic acids extracted from nasopharyngeal swabs. Specific protease cleavage …

0301 basic medicineseverity of diseaseQH301-705.5InflammationPathogenesisCell and Developmental Biology03 medical and health sciences0302 clinical medicineDownregulation and upregulationGenotypemedicinegenetic polymorphismBiology (General)GeneOriginal Researchbusiness.industryConfoundingCOVID-19InflammasomeCell BiologyMERTK030104 developmental biology030220 oncology & carcinogenesisImmunologymedicine.symptombusinessPNPLA3 I148MTLL-1Developmental Biologymedicine.drugFrontiers in Cell and Developmental Biology
researchProduct

New insights into the pathogenesis of giant cell arteritis

2017

Giant cell arteritis (GCA) is an inflammatory chronic disease occurring exclusively in elderly individuals. Until recently, the disease has been considered a unique disease resulting from the interaction in the walls of susceptible arteries, between an unknown infectious agents with local dendritic cells (DCs), activated CD4 T cells and effector macrophages. Recent evidence has shown that this view was too simplistic and has clarified many of the pathogenetic aspects of the disease. Many genetic studies recently published have identified different new genes, including cytokines, adhesion molecules and regulators of innate immunity, as crucial players in the development and progression of GC…

030203 arthritis & rheumatology0301 basic medicineImmunology and Allergy; ImmunologyInnate immune systemGiant Cell ArteritisImmunologyContext (language use)DiseaseBiologymedicine.diseasePathogenesisSettore MED/16 - Reumatologia03 medical and health sciencesGiant cell arteritis030104 developmental biology0302 clinical medicineImmune systemLymphatic systemAntigenImmunologymedicineAnimalsHumansImmunology and Allergyskin and connective tissue diseases
researchProduct

Physiopathologie des vascularites primitives des gros vaisseaux

2016

Giant cell arteritis (GCA) and Takayasu's arteritis (TA) are two granulomatous vasculitis affecting large arteries that present specific epidemiological and clinical features. Their pathogenesis is not fully understood but major advances have been obtained during the last years, thus allowing the emergence of new therapeutic strategies. GCA and TA develop on a specific genetic background but share some similarities regarding the immunological pathways involved in their pathogenesis. The trigger of these diseases is not clearly identified but it is thought that an infectious agent could activate and lead to the maturation of dendritic cells that are localized in the adventitia of arteries. T…

030203 arthritis & rheumatology0301 basic medicineTakayasu's arteritisGastroenterologyBiologymedicine.diseasePathogenesis03 medical and health sciencesGiant cell arteritis030104 developmental biology0302 clinical medicinemedicine.anatomical_structureImmune systemGiant cellAdventitiaImmunologyInternal MedicinemedicineCytotoxic T cellcardiovascular diseasesArteritisLa Revue de Médecine Interne
researchProduct

2019

Viruses frequently spread among cells or hosts in groups, with multiple viral genomes inside the same infectious unit. These collective infectious units can consist of multiple viral genomes inside the same virion, or multiple virions inside a larger structure such as a vesicle. Collective infectious units deliver multiple viral genomes to the same cell simultaneously, which can have important implications for viral pathogenesis, antiviral resistance, and social evolution. However, little is known about why some viruses transmit in collective infectious units, whereas others do not. We used a simple evolutionary approach to model the potential costs and benefits of transmitting in a collect…

0303 health sciencesCancer Research030306 microbiologyvirusesViral pathogenesisAntiviral resistanceBiologyVirologyGenome03 medical and health sciencesInfectious DiseasesMultiplicity of infectionViral replicationViral genomesVirologyViral evolution030304 developmental biologyVirus Research
researchProduct

Genome-wide association study of diabetic kidney disease highlights biology involved in renal basement membrane collagen

2018

Diabetic kidney disease (DKD) is a heritable but poorly understood complication of diabetes. To identify genetic variants predisposing to DKD, we performed genome-wide association analyses in 19,406 individuals with type 1 diabetes (T1D) using a spectrum of DKD definitions basedon albuminuria and renal function. We identified 16 genome-wide significant loci. The variant with the strongest association (rs55703767) is a common missense mutation in the collagen type IV alpha 3 chain(COL4A3)gene, which encodes a major structural component of the glomerular basement membrane (GBM) implicated in heritable nephropathies. The rs55703767 minor allele (Asp326Tyr) is protective against several definit…

0303 health sciencesGlomerular basement membraneRenal function030209 endocrinology & metabolismGenome-wide association studyBiologyurologic and male genital diseasesmedicine.diseaseBioinformatics3. Good healthMinor allele frequencyPathogenesis03 medical and health sciences0302 clinical medicinemedicine.anatomical_structureDiabetes mellitusAlbuminuriamedicineMissense mutationmedicine.symptom030304 developmental biology
researchProduct