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- W2891221448 endingPage "e0203118" @default.
- W2891221448 startingPage "e0203118" @default.
- W2891221448 abstract "Viruses have long been implicated in the pathogenesis of autoimmunity, yet their contribution remains circumstantial partly due to the lack of well-documented information on infections prior to autoimmune disease onset. Here, we used the lymphocytic choriomeningitis virus (LCMV) as a model to mechanistically dissect the impact of viral infection on lupus-like autoimmunity. Virus persistence strongly enhanced disease in mice with otherwise weak genetic predisposition but not in highly predisposed or non-autoimmune mice, indicating a synergistic interplay between genetic susceptibility and virus infection. Moreover, endosomal Toll-like receptors (TLRs) and plasmacytoid dendritic cells (pDCs) were both strictly required for disease acceleration, even though LCMV also induces strong TLR-independent type I interferon (IFN-I) production via RNA helicases and MAVS in conventional DCs. These results suggest that LCMV enhances systemic autoimmunity primarily by providing stimulatory nucleic acids for endosomal TLR engagement, whereas overstimulation of the MAVS-dependent cytosolic pathway in the absence of endosomal TLR signaling is insufficient for disease induction." @default.
- W2891221448 created "2018-09-27" @default.
- W2891221448 creator A5001380638 @default.
- W2891221448 creator A5004663851 @default.
- W2891221448 creator A5020312110 @default.
- W2891221448 creator A5038738015 @default.
- W2891221448 creator A5053511981 @default.
- W2891221448 creator A5088597500 @default.
- W2891221448 date "2018-09-10" @default.
- W2891221448 modified "2023-10-17" @default.
- W2891221448 title "Lupus acceleration by a MAVS-activating RNA virus requires endosomal TLR signaling and host genetic predisposition" @default.
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- W2891221448 doi "https://doi.org/10.1371/journal.pone.0203118" @default.
- W2891221448 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6130858" @default.
- W2891221448 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30199535" @default.
- W2891221448 hasPublicationYear "2018" @default.