https://hdl.handle.net/20.500.11811/1486 Fri, 10 Apr 2026 18:24:00 GMT 2026-04-10T18:24:00Z https://hdl.handle.net/20.500.11811/13361 Mouse models of type I interferonopathies Luca, Domnica; Kato, Hiroki Type I interferonopathies are severe monogenic diseases caused by mutations that result in chronically upregulated production of type I interferon. They present with a broad variety of symptoms, the mechanisms of which are being extensively studied. Mouse models of type I interferonopathies are an important resource for this purpose, and in this context, we review several key molecular and phenotypic findings that are advancing our understanding of the respective diseases. We focus on genotypes related to nucleic acid metabolism, sensing by cytosolic receptors and downstream signalling. Mon, 16 Dec 2024 00:00:00 GMT https://hdl.handle.net/20.500.11811/13361 2024-12-16T00:00:00Z https://hdl.handle.net/20.500.11811/9219 Extracellular vesicles derived from Hepatitis-D Virus infected cells induce a proinflammatory cytokine response in human peripheral blood mononuclear cells and macrophages Jung, Stephanie; Altstetter, Sebastian Maximilian; Wilsch, Florian; Shein, Mikhail; Schütz, Anne Kathrin; Protzer, Ulrike Hepatitis D Virus (HDV) is a satellite virus requiring a Hepatitis B Virus (HBV) envelope proteins for productive infection. Hepatitis D is the most severe form of viral hepatitis and is a global health threat affecting 15 to 20 million humans. In contrast to the Hep atitis B Virus mono-infection, against which only a minor innate immune response is mounted at most, HBV-HDV coinfection is characterized by strong activation of innate immune responses. To shed light on poorly understood mechanisms of HDV-triggered disease progression, we focussed on the question how immune cells may be activated by HDV. We hypothesized that extracellular vesicles (EVs) released from infected cells me diate this activation. We, therefore, purified EVs from the supernatant of HDV-infected and non-infected cells and incubated them with human peripheral blood mononuclear cells (PBMC) and macrophages. Here we show for the first time that HDV infection leads to the production of EVs which subsequently mediate a proinflammatory cytokine response in primary human immune cells. These data might help to understand how HDV can be sensed by non-infected immune cells. Fri, 14 Feb 2020 00:00:00 GMT https://hdl.handle.net/20.500.11811/9219 2020-02-14T00:00:00Z