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TLR3-dependent immune regulatory functions of human mesangial cells

Cellular & Molecular Immunology 2012年第4期9卷 334-340页

作者： Monika Merkle Andrea Ribeiro Simone Koppel joachim pircher Hanna Mannell Maximilian Roeder Markus Wornle Medizinische Poliklinik--Campus Innenstadt Klinikum der LMU Munich Germany Walter-Brendel-Centre of Experimental Medicine University of Munich MunichGermany

In glomerulonephritis, the migration of inflammatory cells into the glomerulus is an important step in disease initiation and progression. The viral receptor Toll-like receptor 3 （TLR3） is known to play a role in virus-associated glomerulonephritis. Based on this knowledge, this study aimed to define the effects of the TLR3 ligand polyriboinosinic：polyribocytidylic acid （poly（hC）） on the expression of adhesion molecules and macrophage colony-stimulating factor （M-CSF） on resident glomerular cells. Experiments in MCs demonstrated that the activation of viral receptors by poly（I.C） leads to a time- and dose-dependent induction of intercellular adhesion molecule 1 （ICAM-1）, vascular cell adhesion molecule 1 （VCAM-1） and M-CSF at both the mRNA and protein levels; these results were confirmed by incubating MCs with HCV RNA. As shown in knockdown experiments, this effect is specifically mediated by TLR3. The prestimulation of MCs with proinfiammatory cytokines increases the effects of poly（hC）, except for its induction of VCAM-I. Tumor-necrosis factor （TNF）-a, likewise, induces ICAM-1, VCAM-1 and M-CSF, and amplifies the mesangial response to poly（hC）. These results were confirmed by incubating MCs with HCV RNA. We thus provide evidence that human MCs represent a potential target of the leukocytes and monocytes that infiltrate the glomerulus in viral disease-associated GN, highlighting the possibility that MCs may act as resident antigen-presenting cells.

关键词： adhesion molecules glomerulonephritis hepatitis C Toll-like receptor 3

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Arterial thrombosis in the context of HCV-associated vascular disease can be prevented by protein C

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Cellular & Molecular Immunology 2017年第12期14卷 986-996页

作者： Philipp Blüm joachim pircher Monika Merkle Thomas Czermak Andrea Ribeiro Hanna Mannell Florian Krötz Alexander Hennrich Michael Spannagl Simone Köppel Erik Gaitzsch Markus Wörnle Medizinische Klinik und Poliklinik IV InnenstadtKlinikum der Universität München80336 MünchenGermany Walter Brendel Centre of Experimental Medicine and Munich Heart Alliance Ludwig Maximilians University München80336 MünchenGermany Medizinische Klinik und Poliklinik I Klinikum der Universität München80336 MünchenGermany Abteilung für Transfusionsmedizin Zelltherapeutika und HämostaseologieKlinikum der Universität München80336 MünchenGermany

Hepatitis C virus(HCV)infection is a major problem *** is not limited to liver disease but is frequently complicated by immune-mediated extrahepatic manifestations such as glomerulonephritis or vasculitis.A fatal complication of HCV-associated vascular disease is ***:polyribocytidylic acid(poly(I:C)),a synthetic analog of viral RNA,induces a Toll-like receptor 3(TLR3)-dependent arteriolar thrombosis without significant thrombus formation in venules in *** procoagulant effects are caused by increased endothelial synthesis of tissue factor and PAI-1 without platelet *** addition to human umbilical endothelial cells(HUVEC),human mesangial cells(HMC)produce procoagulatory factors,cytokines and adhesion molecules after stimulation with poly(I:C)or HCV-containing cryoprecipitates from a patient with a HCV infection as *** protein C(APC)is able to prevent the induction of procoagulatory factors in HUVEC and HMC in vitro and blocks the effects of poly(I:C)and HCV-RNA on the expression of cytokines and adhesion molecules in HMC but not in *** vivo,protein C inhibits poly(I:C)-induced arteriolar ***,endothelial cells are de facto able to actively participate in immune-mediated vascular thrombosis caused by viral ***,we provide evidence for the ability of protein C to inhibit TLR3-mediated arteriolar thrombosis caused by HCV infection.

关键词： hepatitis C thrombosis toll-like receptor 3

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Liver cancer:Targeted future options

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World Journal of Hepatology 2011年第2期3卷 38-44页

作者： Andreas pircher Michael Medinger joachim Drevs Department for Hematology and Oncology Medical University InnsbruckAnichstr.35Innsbruck 6020 Austria Hematology Department University Hospital BaselPetersgraben 4Basel 4031Switzerland Department for Internal Medicine Hematology and OncologyGemeinschaftskrankenhaus HerdeckeGerhard-Kienle-Weg 4Herdecke 58313Germany

Hepatocellular carcinoma(HCC)has a poor prognosis an d systemic chemotherapies have disappointing *** increasing knowledge of the molecular biolog y of HCC has resulted in novel targets,with the vascular endothelial growth factor and epidermal growth factor receptor(EGFR)-related pathways being of special *** blood vessel formation(angiogenesis)is essential for the growth of solid ***-angiogenic strategies have become an important therapeutic modality for solid *** agents targeting angiogenesis-related pathways have entered clinical trials or have been already approved for the treatment of solid *** include monoclonal antibodies,receptor tyrosine kinase inhibitors and immunomodulatory *** is a highly vascular tumor,and angiogenesis is be-lieved to play an important role in its development and *** review summarizes recent advances in the basic understanding of the role of angiogenesis in HCC as well as clinical trials with novel therapeutic approaches targeting angiogenesis and EGFR-related pathways.

关键词： Angiogenesis Epidermal growth factor receptor Hepatocellular carcinoma Targeted therapy Vascular endothelial growth factor

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