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Projekt Druckansicht

Kontrolle von HSV-1 spezifischen Replikations- und Transmissions-Mechanismen in humanen Dendritischen Zellen

Fachliche Zuordnung Immunologie
Förderung Förderung von 2018 bis 2022
Projektkennung Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 398064017
 
Erstellungsjahr 2022

Zusammenfassung der Projektergebnisse

In summary, in our view project was a very successful leading to new and unexpected data, including the fact that autophagic degradation of lamins is essential for the nuclear egress of HSV-1 and that mDC hamper this process, by upregulating KIF1B and KIF2A molecules, and thereby inhibiting the generation of mature infectious viral particles. In addition, we found that HSV-1 derived L-particles modulate the phenotype and stimulatory function of mDCS. Furthermore, targeting IL-6 R expression by HSV-1 on mDCs has been identified as a new viral immune escape mechanism. Finally, we provide data showing that HSV-2 interferes with DC migration and therefore the induction of potent antiviral immune responses. Work regarding mechanisms related to CD83 degradation and the functional ligand studies are still ongoing.

Projektbezogene Publikationen (Auswahl)

 
 

Zusatzinformationen

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