0000000000041462

AUTHOR

E. Löser

showing 3 related works from this author

IL-10 down-regulates T cell activation by antigen-presenting liver sinusoidal endothelial cells through decreased antigen uptake via the mannose rece…

1998

SUMMARYOur study demonstrates that antigen-presenting liver sinusoidal endothelial cells (LSEC) induce production of interferon-gamma (IFN-γ) from cloned Th1 CD4+ T cells. We show that LSEC used the mannose receptor for antigen uptake, which further strengthened the role of LSEC as antigen-presenting cell (APC) population in the liver. The ability of LSEC to activate cloned CD4+ T cells antigen-specifically was down-regulated by exogenous prostaglandin E2 (PGE2) and by IL-10. We identify two separate mechanisms by which IL-10 down-regulated T cell activation through LSEC. IL-10 decreased the constitutive surface expression of MHC class II as well as of the accessory molecules CD80 and CD86 …

Liver cytologyT cellT-LymphocytesImmunologyAntigen presentationAntigen-Presenting CellsDown-RegulationReceptors Cell SurfaceBiologyLymphocyte ActivationDinoprostoneMiceAntigenAntigens CDmedicineImmunology and AllergyAnimalsLectins C-TypeCD86Antigen PresentationMice Inbred BALB CMembrane GlycoproteinsHistocompatibility Antigens Class IIOriginal ArticlesInterleukin-10Interleukin 10medicine.anatomical_structureMannose-Binding LectinsLiverImmunologyB7-1 AntigenCytokinesFemaleB7-2 AntigenEndothelium VascularMannoseCD80Mannose receptorMannose ReceptorClinical and experimental immunology
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Regulation of endotoxin-induced IL-6 production in liver sinusoidal endothelial cells and Kupffer cells by IL-10

1997

SUMMARY Sinusoidal endothelial cells and Kupffer cells are the first cell populations in the liver that come into contact with gut-derived endotoxin in portal blood. Although endotoxin concentrations as high as 1 ng/ml are physiologically present in portal blood, no local inflammation is seen. We show that the proinflammatory cytokine IL-6, which is central to the development of inflammatory reactions in the liver, is produced by sinusoidal endothelial cells and Kupffer cells in response to low concentrations of endotoxin (100 pg/ml to 1 ng/ml). The anti-inflammatory cytokine IL-10 down-regulated endotoxin-induced IL-6 release in endothelial and Kupffer cells. Importantly, Kupffer cells sec…

medicine.medical_specialtyEndotheliumKupffer Cellsmedicine.medical_treatmentImmunologyInflammationBiologyProinflammatory cytokineMiceInternal medicinemedicineAnimalsImmunology and AllergyInterleukin 4Mice Inbred BALB CInterleukin-6MicrocirculationKupffer cellOriginal ArticlesInterleukin-10EndotoxinsEndothelial stem cellInterleukin 10medicine.anatomical_structureCytokineEndocrinologyLiverImmunologyEndothelium Vascularmedicine.symptomClinical and Experimental Immunology
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Role of sinusoidal endothelial cells of the liver in concanavalin A-induced hepatic injury in mice

1996

CD4+ T lymphocytes have been identified as being responsible for organ damage in the murine model of experimental liver injury induced by intravenous injection of concanavalin A (Con A). Liver sinusoidal endothelial cells (SEC) and Kupffer's cells (KC) are among the first cells that come into contact with lymphocytes in the liver sinusoid. We aimed to investigate the respective role of these cell populations in the initial steps of T-cell-mediated liver injury in Con A-induced hepatitis. By electron microscopy, we could show that intravenously applied Con A bound predominantly to SEC but not to KC. KC depletion by gadolinium chloride treatment of mice did not result in protection from liver…

Liver sinusoidLiver injuryPathologymedicine.medical_specialtyHepatologybiologyStimulationAutoimmune hepatitismedicine.diseaseMolecular biologyIn vitromedicine.anatomical_structureConcanavalin Amedicinebiology.proteinTumor necrosis factor alphaCytotoxicityHepatology
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