Search results for "Chemokine CCL1"

showing 4 items of 14 documents

Compartmentalized production of CCL17 in vivo: strong inducibility in peripheral dendritic cells contrasts selective absence from the spleen.

2003

Dendritic cells (DCs)(*) fulfill an important regulatory function at the interface of the innate and adaptive immune system. The thymus and activation-regulated chemokine (TARC/CCL17) is produced by DCs and facilitates the attraction of activated T cells. Using a fluorescence-based in vivo reporter system, we show that CCL17 expression in mice is found in activated Langerhans cells and mature DCs located in various lymphoid and nonlymphoid organs, and is up-regulated after stimulation with Toll-like receptor ligands. DCs expressing CCL17 belong to the CD11b(+)CD8(-)Dec205(+) DC subset, including the myeloid-related DCs located in the subepithelial dome of Peyer's patches. CCL17-deficient mi…

LipopolysaccharidesLymphoid TissueGreen Fluorescent ProteinsDermatitis ContactArticleMicePhagocytosisGenes ReporterAnimalsListeriosisdendritic cellsCCL17/TARCcontact hypersensitivityMice Knockoutintegumentary systemGraft Survivaltransplant rejectionrespiratory systemCD11c AntigenToll-like receptorsMice Inbred C57BLLuminescent ProteinsEpidermal CellsChemokines CCLangerhans CellsGene TargetingHeart TransplantationChemokine CCL17EpidermisSpleenThe Journal of experimental medicine
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Loss of p53 Attenuates the Contribution of IL-6 Deletion on Suppressed Tumor Progression and Extended Survival in Kras-Driven Murine Lung Cancer

2013

Interleukin-6 (IL-6) is involved in lung cancer tumorigenesis, tumor progression, metastasis, and drug resistance. Previous studies show that blockade of IL-6 signaling can inhibit tumor growth and increase drug sensitivity in mouse models. Clinical trials in non-small cell lung cancer (NSCLC) reveal that IL-6 targeted therapy relieves NSCLC-related anemia and cachexia, although other clinical effects require further study. We crossed IL-6(-/-) mice with Kras(G12D) mutant mice, which develop lung tumors after activation of mutant Kras(G12D), to investigate whether IL-6 inhibition contributes to tumor progression and survival time in vivo. Kras(G12D); IL-6(-/-) mice exhibited increased tumor…

Lung Neoplasmsmedicine.medical_treatmentlcsh:Medicinemedicine.disease_causeMetastasisTargeted therapyMice0302 clinical medicineCarcinoma Non-Small-Cell LungNeoplasm MetastasisPhosphorylationlcsh:Science0303 health sciencesMultidisciplinary3. Good healthGene Expression Regulation Neoplastic030220 oncology & carcinogenesisDisease ProgressionKRASResearch ArticleSignal TransductionSTAT3 Transcription FactorMice TransgenicBiologyProto-Oncogene Proteins p21(ras)03 medical and health sciencesFLOXmedicineAnimalsHumansLung cancerneoplasms030304 developmental biologyChemokine CCL20Interleukin-6Tumor Necrosis Factor-alphalcsh:RCancermedicine.diseaseSurvival Analysisdigestive system diseasesrespiratory tract diseasesDisease Models AnimalTumor progressionMutationCancer researchChemokine CCL19lcsh:QTumor Suppressor Protein p53CarcinogenesisPLoS ONE
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The density and type of MECA-79-positive high endothelial venules correlate with lymphocytic infiltration and tumour regression in primary cutaneous …

2013

Aims Tumour-infiltrating lymphocytes have prognostic value in malignant melanoma. High endothelial venules (HEVs) are specialized vessels present in lymph nodes and tertiary lymphoid organs. CCL19, CCL21 and CCR7 regulate lymphocyte migration through HEVs. The aim of our study was to correlate HEV density in cutaneous primary and metastatic malignant melanomas with clinicopathological parameters, and with CCL19, CCL21 and CCR7 mRNA expression. Methods and results High endothelial venule density was evaluated by immunohistochemistry with a specific antibody, MECA-79, and chemokine expression was evaluated by real-time PCR. MECA-79-positive vessels, covered by cuboidal (C-HEV) or flat (F-HEV)…

MaleReceptors CCR7Pathologymedicine.medical_specialtySkin NeoplasmsHistologyEndotheliumvirusesHigh endothelial venulesC-C chemokine receptor type 7BiologyPathology and Forensic MedicineLymphocytes Tumor-InfiltratingmedicineHumansRNA MessengerRNA NeoplasmMelanomaLymphatic VesselsRetrospective StudiesChemokine CCL21MelanomaMembrane Proteinsvirus diseasesGeneral MedicineMiddle AgedPrognosismedicine.diseaseImmunohistochemistrydigestive system diseasesLymphatic systemmedicine.anatomical_structureAntigens SurfaceCutaneous melanomaChemokine CCL19ImmunohistochemistryFemaleCCL21Histopathology
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Thyroid hormone induction of the adrenoleukodystrophy-related gene (ABCD2).

2003

X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VLCFA) beta-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3'-tri-iodothyronine (T3) receptor (TRbeta) as a heterodimer and mediating T3 responsiveness of ABCD2 in its promoter conte…

MaleThyroid HormonesReceptors Retinoic AcidGene ExpressionATP-binding cassette transporterRetinoid X receptorRats Sprague-DawleyMiceABCD3Gene expressionABCD2medicineAnimalsHumansReceptorAdrenoleukodystrophyPromoter Regions GeneticGeneCells CulturedRepetitive Sequences Nucleic AcidPharmacologyChemokine CCL22Mice KnockoutReceptors Thyroid Hormonebiologymedicine.diseaseCell biologyRatsUp-RegulationOligodendrogliaRetinoid X ReceptorsLiverAstrocytesChemokines CCbiology.proteinCancer researchMolecular MedicineTriiodothyronineAdrenoleukodystrophyChemokine CCL17Transcription FactorsMolecular pharmacology
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