29 results on '"R Bröring"'
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2. Kaltlagerung und Kryokonservierung primärer humaner Hepatozyten in modifizierter TiProtec®-Lösung
3. Das Oberflächenantigen (HBsAg) des Hepatitis-B-Virus (HBV) inhibiert eine replikationsabhängige Interferon Antwort im transgenen HBV-Mausmodell
4. Patienten mit einer Virushepatitis weisen eine Induktion in der hepatische Expression der Proteasom alpha-Untereinheit Typ-6 (PSMA6) auf, welche wiederum die Expression proviraler Wirtsgene der Hepatitis-C-Virus-Infektion reguliert
5. Toll-like receptor-activated primary human hepatocytes produce inflammatory cytokines and different types of interferon, resulting in HCV suppression in a co-culture model
6. In vivo treatment with nanolipid-formulated siRNAs targeting ISG15 leads to enhanced responsiveness to interferon in primary hepatocytes
7. Toll-like receptor-activated primary human hepatocytes produce inflammatory cytokines and different types of interferon, resulting in HCV suppression in vitro
8. Hepatic toll-like receptors can be activated by application of siRNAs in vivo via MyD88-dependent pathways which can be controlled by chemical ribose modifications of the siRNA backbone
9. Presence of primary human hepatocytes inhibits expansion of virus-specific CD8+ T cells in vitro
10. In Vivo Treatment With Nanolipid-Formulated siRNAs Targeting ISG15 Leads to Enhanced TLR-Induced Expression of Interferon-Sensitive Genes in Hepatocytes
11. The non-specific activation of liver tissue by siRNAs in vivo can be controlled by chemical ribose modifications of siRNAs
12. The production of interferons is not impaired in primary isolated liver cells from HCV-positive individuals after Toll-like receptor mediated stimulation
13. HBsAg is a potent suppressor of Toll-like receptor mediated innate and adaptive immune responses in liver cells and PBMC
14. The activation of the hepatic innate immune system by siRNA is controlled by chemical modifications and may involve endosomal Toll-like receptors
15. HCV/TLR3-dependent innate and adaptive immune functions of non-parenchymal liver cells are controlled by interleukin-10 and transforming growth factor beta
16. Correlation of type I, -II and -III interferon expression in the liver with clinical and viral parameters in chronic HCV infection
17. Das Interferon-sensitive Gen 15 (ISG15) hat eine provirale Funktion im Rahmen der Hepatitis C Virus Infektion
18. The interferon stimulated gene 15 functions as a proviral factor for HCV and is enhanced in the liver of patients with genotype 1
19. Toll-like receptor signalling in non-parenchymal liver cells is modulated by dexamethasone
20. Dexamethasone is a potent modulator of Toll-like receptor mediated activation of non-parenchymal liver cells
21. Suppression of Hepatitis C Virus replication in vitro is mediated by TLR3- or TLR4-stimulated non-parenchymal liver cells
22. TLR–3 stimulated non-parenchymal liver cells are potent suppressors of HCV replication
23. Funktion von CEACAM-1 im Rahmen der Therapie der Hepatitis C-Virus Infektion mit Interferon-alpha in vivo und in vitro
24. Differentielle Funktion von CEACAM–1 im Rahmen der Therapie der Hepatitis C-Virus Infektion mit Interferon-alpha in vivo und in vitro
25. Mo1537 TLR3-Dependent Immunological Properties of Liver Cells are Controlled by Anti-Inflammatory Cytokines Through Modulation of miR-155 Expression
26. Mo1538 Hepatitis B Virus Surface Antigen Suppresses Innate and Adaptive Immune Responses of Murine and Human Liver Cells
27. Mo1536 Human Hepatocytes Produce Inflammatory Cytokines and Type I, II and III Interferons in Response to Toll-Like Receptor Activation, Resulting in IFN-λ-Mediated Suppression of HCV In Vitro
28. 128 TOLL-LIKE RECEPTOR-ACTIVATED HUMAN HEPATOCYTES PRODUCE INFLAMMATORY CYTOKINES AND TYPE III INTERFERONS, RESULTING IN IFN-γ-MEDIATED SUPPRESSION OF HCV IN VITRO
29. The Toll-Like Receptor Mediated Induction of Interferons is Not Impaired in Primary Liver Cells From HCV-Positive Patients
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