IndraLab
Statements
reach
"Lacking of USP18 leads to an increase signaling of IFN-I, IFN-III, TNF-α and high levels of conjugated ISG15Figure 3: Role of USP18-dependent enforced viral replication in activation of the adaptive immune system and onset of diabetes mellitus type I. (a) USP18 inhibits IFNAR signaling, which leads to enforced viral replication in CD169+ macrophages."
reach
"For example, USP18 is known to prevent IFNAR activation as shown by Honke et al. where USP-18 secreting CD169 macrophages displayed a lower type I IFN sensitivity upon viral infection [38], [57].4
Strategies to control innate immune activation upon conventional and self-amplifying mRNA delivery."
sparser
"Furthermore, Usp18 functions in the type I IFN pathway by down-regulating the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway independently of its isopeptidase activity through an interaction between Usp18 and the IFNAR2 subunit of the type I IFN receptor complex, while neither IFNAR1 nor IFNGR1 (type II IFN) receptor subunits were able to interact with Usp18 ( xref )."
sparser
"Furthermore, Usp18 functions in the type I IFN pathway by down-regulating the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway independently of its isopeptidase activity through an interaction between Usp18 and the IFNAR2 subunit of the type I IFN receptor complex, while neither IFNAR1 nor IFNGR1 (type II IFN) receptor subunits were able to interact with Usp18 ( xref )."