J. Rehwinkel

This study examines how different type I interferons affect signaling and gene expression in human immune cells, finding that responses vary in magnitude but not qualitatively.

This study identifies MxB as an interferon-inducible GTPase that disassembles herpesvirus capsids, promoting genome release and enhancing innate immune responses.

The paper shows hypoxia reduces mitochondrial double-stranded RNA production in breast cancer cells, leading to decreased type I IFN signaling and immunosuppression.

This study identifies a ZBP1-RIPK1-RIPK3 pathway that promotes SARS-CoV-2-induced cytokine expression through inflammatory signaling independent of cell death.

The paper identifies MDA5 as a cellular sensor for SARS-CoV-2 infection that induces type I and III interferons in Calu-3 cells.

This study shows that ADAR1's Z domain prevents IFN responses by recognizing Z-RNA, and its absence leads to spontaneous IFN induction and improved viral control.

The paper identifies NRF2 agonists 4-OI and DMF as inhibitors of SARS-CoV2 replication and inflammatory responses, effective against multiple viruses.

The paper shows that ZBP1 sensing of endogenous nucleic acids causes necroptosis and skin inflammation in RIPK1-deficient keratinocytes, linked to IL-17 immune responses.

This paper shows that SAMHD1 protects cells from dGTP toxicity caused by forodesine, and that forodesine can selectively kill SAMHD1-deficient leukemia cells.

This study identifies ORF9 as a VZV protein that inhibits the cGAS/STING pathway, reducing type I IFN production during infection.

The paper identifies type-1 IFN-primed monocytes as key drivers of fibrosis in IPF, showing their increased levels, altered phenotype, and potential as therapeutic targets.

This study shows that incorporating cGAMP into virus-like particles (VLPs) enhances their immunogenicity, leading to stronger T cell responses and antibody titres against HIV and influenza viruses.

This study shows hypoxia reduces type I IFN pathway activity in cancer cells through transcriptional and chromatin changes, independent of HIF1/2.