Search results for "N-2"

showing 10 items of 1881 documents

Immunological Probes for the Bradykinin B2 Receptor. A Toolbox

1997

Publisher Summary This chapter provides an overview of the immunological tools for bradykinin (BK) B 2 receptor. Receptors for kinins are classified as two major subtypes, B 1 and B 2 , although other subtypes may exist. B 1 receptors are activated by carboxyterminally truncated kinins, whereas BK and kallidin (Lys-BK) are B 2 receptor agonists. Molecular cloning has revealed the primary structures of B 1 and B 2 receptors and identified them as members of the G protein-coupled receptor family, characterized by seven membrane-spanning α-helices. In some tissues, B 1 receptor expression is induced by cytokines, such as interleukin-1, whereas the B 2 receptor is thought to be expressed consti…

Interleukin-21 receptorReceptor expressionB-cell receptor5-HT5A receptorImmune receptorGABBR1BiologyBradykinin receptorMolecular biologyProtease-activated receptor 2
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Molecular and pro-inflammatory aspects of COVID-19: The impact on cardiometabolic health

2022

Obesity, type 2 diabetes (T2DM), hypertension (HTN), and Cardiovascular Disease (CVD) often cluster together as "Cardiometabolic Disease" (CMD). Just under 50% of patients with CMD increased the risk of morbidity and mortality right from the beginning of the COVID-19 pandemic as it has been reported in most countries affected by the SARS-CoV2 virus. One of the pathophysiological hallmarks of COVID-19 is the overactivation of the immune system with a prominent IL-6 response, resulting in severe and systemic damage involving also cytokines such as IL2, IL4, IL8, IL10, and interferon-gamma were considered strong predictors of COVID-19 severity. Thus, in this mini-review, we try to describe the…

Interleukin-6SARS-CoV-2Interleukin-8COVID-19COVID Cardiometabolic Diabetes Inflammation MolecularInterleukin-10Interferon-gammaAdipokinesDiabetes Mellitus Type 2Cardiovascular DiseasesCytokinesHumansInterleukin-2RNA ViralMolecular MedicineInterleukin-4ObesityPandemicsMolecular BiologyBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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CCDC 235538: Experimental Crystal Structure Determination

2004

Related Article: J.Vicente, J.-A.Abad, F.S.Hernandez-Mata, B.Rink, P.G.Jones, M.C.R.de Arellano|2004|Organometallics|23|1292|doi:10.1021/om0342964

Iodo-(26-dimethylphenylisocyano)-(25-bis(13-dithiolan-2-yl)-alpha-(26-dimethylphenylimino)benzyl-S)-palladium dichloromethane solvateSpace GroupCrystallographyCrystal SystemCrystal StructureCell ParametersExperimental 3D Coordinates
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Langerhans Cells Prevent Autoimmunity via Expansion of Keratinocyte Antigen-Specific Regulatory T Cells

2017

Langerhans cells (LCs) are antigen-presenting cells in the epidermis whose roles in antigen-specific immune regulation remain incompletely understood. Desmoglein 3 (Dsg3) is a keratinocyte cell-cell adhesion molecule critical for epidermal integrity and an autoantigen in the autoimmune blistering disease pemphigus. Although antibody-mediated disease mechanisms in pemphigus are extensively characterized, the T cell aspect of this autoimmune disease still remains poorly understood. Herein, we utilized a mouse model of CD4+ T cell-mediated autoimmunity against Dsg3 to show that acquisition of Dsg3 and subsequent presentation to T cells by LCs depended on the C-type lectin langerin. The lack of…

Keratinocytes0301 basic medicineLangerinRegulatory T cellT celllcsh:MedicineAutoimmunitymedicine.disease_causeT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyAutoimmunity03 medical and health sciencesAutoimmune diseasemedicineAnimalsLectins C-TypeAntigenseducationCell ProliferationAutoimmune diseaselcsh:R5-920Antigen Presentationeducation.field_of_studyDesmoglein 3integumentary systembiologylcsh:RHistocompatibility Antigens Class IIPeripheral toleranceReceptors Interleukin-2Regulatory T cellsGeneral Medicinemedicine.diseaseCell biologyMice Inbred C57BLPemphigusMannose-Binding Lectins030104 developmental biologymedicine.anatomical_structureLangerhans CellsAntigens SurfaceDesmoglein 3biology.proteinlcsh:Medicine (General)PemphigusResearch PaperSignal TransductionEBioMedicine
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Epigenetic control of IL-23 expression in keratinocytes is important for chronic skin inflammation

2018

The chronic skin inflammation psoriasis is crucially dependent on the IL-23/IL-17 cytokine axis. Although IL-23 is expressed by psoriatic keratinocytes and immune cells, only the immune cell-derived IL-23 is believed to be disease relevant. Here we use a genetic mouse model to show that keratinocyte-produced IL-23 is sufficient to cause a chronic skin inflammation with an IL-17 profile. Furthermore, we reveal a cell-autonomous nuclear function for the actin polymerizing molecule N-WASP, which controls IL-23 expression in keratinocytes by regulating the degradation of the histone methyltransferases G9a and GLP, and H3K9 dimethylation of the IL-23 promoter. This mechanism mediates the inducti…

KeratinocytesMale0301 basic medicinemedicine.medical_treatmentWiskott-Aldrich Syndrome Protein NeuronalGeneral Physics and AstronomyEpigenesis GeneticHistonesMice0302 clinical medicineGenes ReporterInterleukin 23Promoter Regions Geneticlcsh:ScienceSkinMice KnockoutMultidisciplinaryInterleukin-17QMiddle AgedCytokine030220 oncology & carcinogenesisHistone methyltransferaseTumor necrosis factor alphaSignal transductionmedicine.symptomSignal TransductionAdultScienceGreen Fluorescent ProteinsPrimary Cell CultureInflammationBiologyArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesImmune systemPsoriasismedicineAnimalsHumansPsoriasisInflammationHistone-Lysine N-MethyltransferaseGeneral Chemistrybiochemical phenomena metabolism and nutritionmedicine.diseaseDisease Models AnimalHEK293 Cells030104 developmental biologyInterleukin-23 Subunit p19Cancer researchlcsh:QNature Communications
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Langerinneg conventional dendritic cells produce IL-23 to drive psoriatic plaque formation in mice.

2013

Psoriasis is an autoinflammatory skin disease of unknown etiology. Topical application of Aldara cream containing the Toll-like receptor (TLR)7 agonist Imiquimod (IMQ) onto patients induces flares of psoriasis. Likewise, in mice IMQ triggers pathological changes closely resembling psoriatic plaque formation. Key cytokines like IL-23 and type-I IFN (IFN-I), both being produced mainly by dendritic cells (DCs), have been implicated in psoriasis. Although plasmacytoid DCs (pDCs) are the main source of IFNα and thought to initiate disease, conventional DCs (cDCs) appear to maintain the psoriatic lesions. Any role of cDCs during lesion formation remains elusive. Here, we report that selective ac…

LangerinCD11c610 Medicine & healthInflammation10263 Institute of Experimental ImmunologyInterleukin-23Mice03 medical and health sciences0302 clinical medicinePsoriasismedicineInterleukin 23AnimalsPsoriasisLectins C-Type030304 developmental biologyMice Knockout1000 Multidisciplinary0303 health sciencesImiquimodMembrane GlycoproteinsMultidisciplinarybiologyintegumentary systemhemic and immune systemsDendritic cellTLR7Biological SciencesAcquired immune systemmedicine.disease3. Good healthDisease Models AnimalMannose-Binding LectinsToll-Like Receptor 7Langerhans Cells030220 oncology & carcinogenesisAntigens SurfaceMyeloid Differentiation Factor 88ImmunologyAminoquinolinesbiology.protein570 Life sciences; biologymedicine.symptom
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Clusterin and LRP2 are critical components of the hypothalamic feeding regulatory pathway.

2012

Hypothalamic feeding circuits are essential for the maintenance of energy balance. There have been intensive efforts to discover new biological molecules involved in these pathways. Here we report that central administration of clusterin, also called apolipoprotein J, causes anorexia, weight loss and activation of hypothalamic signal transduction-activated transcript-3 in mice. In contrast, inhibition of hypothalamic clusterin action results in increased food intake and body weight, leading to adiposity. These effects are likely mediated through the mutual actions of the low-density lipoprotein receptor-related protein-2, a potential receptor for clusterin, and the long-form leptin receptor…

LeptinMaleSTAT3 Transcription Factormedicine.medical_specialtyApolipoprotein BHypothalamusGeneral Physics and AstronomyGeneral Biochemistry Genetics and Molecular BiologyCell LineMiceInternal medicinemedicineAnimalsHumansObesityPhosphorylationReceptorInjections IntraventricularEpididymisMultidisciplinaryLeptin receptorbiologyClusterinLeptinBody WeightGeneral ChemistryFeeding BehaviorLRP2ImmunohistochemistryHedgehog signaling pathwayAnorexiaRatsLow Density Lipoprotein Receptor-Related Protein-2EndocrinologyClusterinStarvationbiology.proteinReceptors LeptinLipoproteinProtein BindingSignal TransductionNature communications
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Phenolic-glycolipid-1 and lipoarabinomannan preferentially modulate TCR- and CD28-triggered proximal biochemical events, leading to T-cell unresponsi…

2012

Abstract Background Advanced stages of leprosy show T cell unresponsiveness and lipids of mycobacterial origin are speculated to modulate immune responses in these patients. Present study elucidates the role of phenolicglycolipid (PGL-1) and Mannose-capped lipoarabinomannan (Man-LAM) on TCR- and TCR/CD28- mediated signalling. Results We observed that lipid antigens significantly inhibit proximal early signalling events like Zap-70 phosphorylation and calcium mobilization. Interestingly, these antigens preferentially curtailed TCR-triggered early downstream signalling events like p38 phosphorylation whereas potentiated that of Erk1/2. Further, at later stages inhibition of NFAT binding, IL-2…

LipopolysaccharidesEndocrinology Diabetes and MetabolismT-LymphocytesClinical BiochemistryPGL-1Man-LAMGene ExpressionLymphocyte ActivationJurkat cellsJurkat CellsEndocrinologyT-cell activationIL-2 receptorPhosphorylationExtracellular Signal-Regulated MAP KinasesPromoter Regions Geneticlcsh:RC620-627Protein Kinase CImmunity CellularZAP-70 Protein-Tyrosine KinaseCD28hemic and immune systemsCell biologyMycobacterium lepraelcsh:Nutritional diseases. Deficiency diseasesmedicine.anatomical_structureHost-Pathogen InteractionsProtein BindingMAP Kinase Signaling SystemT cellReceptors Antigen T-Cellchemical and pharmacologic phenomenaBiologyImmune systemCD28 AntigensLeprosymedicineHumansSecretionCalcium SignalingCell ProliferationBiochemistry medicalAntigens BacterialLipoarabinomannanNFATC Transcription FactorsResearchBiochemistry (medical)T-cell receptorInterleukin-2 Receptor alpha SubunitMycobacteriaGene Expression RegulationAnergyImmunologyLeukocytes MononuclearInterleukin-2GlycolipidsLipids in Health and Disease
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Phenolic Substances from Phagnalon rupestre Protect against 2,4,6-Trinitrochlorobenzene-Induced Contact Hypersensitivity

2011

2-isoprenylhydroquinone-1-glucoside (1), 3,5-dicaffeoylquinic acid (2), and 3,5-dicaffeoylquinic acid methyl ester (3), isolated from Phagnalon rupestre, improved the contact hypersensitivity response to 2,4,6-trinitrochlorobenzene in mice. These phenolics reduced ear swelling and IL-1β content by 50% 24 h after challenge; in addition, 2 inhibited tumor necrosis factor-α by 53%. All three compounds also reduced interleukin-2 content by 50% 72 h after challenge. Both 2 and 3 inhibited metalloproteinase-9 levels in the skin lesions by 66% and 41%, respectively, and lowered cyclooxygenase-2 expression by 44% and 49%, respectively, at 24 h. Moreover, 2 was effective against atopic dermatitis in…

LipopolysaccharidesInterleukin-1betaPharmaceutical SciencePicryl ChloridePharmacognosyDermatitis ContactAnalytical ChemistryMicechemistry.chemical_compoundPhenolsDrug DiscoverymedicineAnimalsEdemaPhenolsSkinPharmacologychemistry.chemical_classificationCyclooxygenase 2 InhibitorsDose-Response Relationship DrugTraditional medicineTumor Necrosis Factor-alphaMacrophagesOrganic ChemistryContact hypersensitivityGlycosidePhagnalon rupestreEarmedicine.diseaseDisease Models AnimalComplementary and alternative medicineBiochemistrychemistryInterleukin-2Molecular MedicineContact dermatitisJournal of Natural Products
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CD11c+ Alveolar Macrophages are a Source of IL-23 During Lipopolysaccharide-Induced Acute Lung Injury

2013

Acute lung injury (ALI) is a severe pulmonary disease causing high numbers of fatalities worldwide. Innate immune responses are an integral part of the pathophysiologic events during ALI. Interleukin 23 (IL-23) is a proinflammatory mediator known to direct the inflammatory responses in various settings of infection, autoimmunity, and cancer. Interleukin 23 has been associated with proliferation and effector functions in T(H)17 cells. Surprisingly, little is known about production of IL-23 during ALI. In this study, we found expression of mRNA for IL-23p19 to be 10-fold elevated in lung homogenates of C57BL/6 mice after lipopolysaccharide (LPS)-induced ALI. Likewise, concentrations of IL-23 …

LipopolysaccharidesMaleLipopolysaccharideAcute Lung InjuryCD11cBiologyLung injuryCritical Care and Intensive Care MedicineInterleukin-23ArticleProinflammatory cytokineMicechemistry.chemical_compoundMacrophages AlveolarmedicineAnimalsInnate immune systemmedicine.diagnostic_testrespiratory systemCD11c Antigenrespiratory tract diseasesBronchoalveolar lavagechemistryImmunologyEmergency MedicineAlveolar macrophageInterleukin 17Shock
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