Matches in SemOpenAlex for { <https://semopenalex.org/work/W2121525530> ?p ?o ?g. }
- W2121525530 endingPage "e1004086" @default.
- W2121525530 startingPage "e1004086" @default.
- W2121525530 abstract "The type I interferon (IFN) signaling response limits infection of many RNA and DNA viruses. To define key cell types that require type I IFN signaling to orchestrate immunity against West Nile virus (WNV), we infected mice with conditional deletions of the type I IFN receptor (IFNAR) gene. Deletion of the Ifnar gene in subsets of myeloid cells resulted in uncontrolled WNV replication, vasoactive cytokine production, sepsis, organ damage, and death that were remarkably similar to infection of Ifnar−/− mice completely lacking type I IFN signaling. In Mavs−/−×Ifnar−/− myeloid cells and mice lacking both Ifnar and the RIG-I-like receptor adaptor gene Mavs, cytokine production was muted despite high levels of WNV infection. Thus, in myeloid cells, viral infection triggers signaling through MAVS to induce proinflammatory cytokines that can result in sepsis and organ damage. Viral pathogenesis was caused in part by massive complement activation, as liver damage was minimized in animals lacking complement components C3 or factor B or treated with neutralizing anti-C5 antibodies. Disease in Ifnar−/− and CD11c Cre+Ifnarf/f mice also was facilitated by the proinflammatory cytokine TNF-α, as blocking antibodies diminished complement activation and prolonged survival without altering viral burden. Collectively, our findings establish the dominant role of type I IFN signaling in myeloid cells in restricting virus infection and controlling pathological inflammation and tissue injury." @default.
- W2121525530 created "2016-06-24" @default.
- W2121525530 creator A5002746624 @default.
- W2121525530 creator A5005113342 @default.
- W2121525530 creator A5007558296 @default.
- W2121525530 creator A5008491017 @default.
- W2121525530 creator A5016005915 @default.
- W2121525530 creator A5031713882 @default.
- W2121525530 creator A5031994519 @default.
- W2121525530 creator A5032376386 @default.
- W2121525530 creator A5044391826 @default.
- W2121525530 creator A5049817365 @default.
- W2121525530 creator A5065618624 @default.
- W2121525530 date "2014-04-17" @default.
- W2121525530 modified "2023-10-17" @default.
- W2121525530 title "Deficient IFN Signaling by Myeloid Cells Leads to MAVS-Dependent Virus-Induced Sepsis" @default.
- W2121525530 cites W1488091068 @default.
- W2121525530 cites W1488854843 @default.
- W2121525530 cites W1519801500 @default.
- W2121525530 cites W1529674879 @default.
- W2121525530 cites W1590582894 @default.
- W2121525530 cites W1592616574 @default.
- W2121525530 cites W1595293335 @default.
- W2121525530 cites W1766009520 @default.
- W2121525530 cites W1960041676 @default.
- W2121525530 cites W1967575570 @default.
- W2121525530 cites W1970136118 @default.
- W2121525530 cites W1975075325 @default.
- W2121525530 cites W1990130249 @default.
- W2121525530 cites W1993712001 @default.
- W2121525530 cites W1997572777 @default.
- W2121525530 cites W1998473333 @default.
- W2121525530 cites W2003828813 @default.
- W2121525530 cites W2010444790 @default.
- W2121525530 cites W2010480258 @default.
- W2121525530 cites W2018071918 @default.
- W2121525530 cites W2018722698 @default.
- W2121525530 cites W2020173029 @default.
- W2121525530 cites W2021655479 @default.
- W2121525530 cites W2022630488 @default.
- W2121525530 cites W2025471246 @default.
- W2121525530 cites W2028357619 @default.
- W2121525530 cites W2032894542 @default.
- W2121525530 cites W2035541724 @default.
- W2121525530 cites W2035873332 @default.
- W2121525530 cites W2036679352 @default.
- W2121525530 cites W2038558750 @default.
- W2121525530 cites W2046413321 @default.
- W2121525530 cites W2051329301 @default.
- W2121525530 cites W2053466821 @default.
- W2121525530 cites W2055972388 @default.
- W2121525530 cites W2057345517 @default.
- W2121525530 cites W2058756509 @default.
- W2121525530 cites W2060926084 @default.
- W2121525530 cites W2068503190 @default.
- W2121525530 cites W2069115249 @default.
- W2121525530 cites W2070026001 @default.
- W2121525530 cites W2073760661 @default.
- W2121525530 cites W2076028337 @default.
- W2121525530 cites W2076198632 @default.
- W2121525530 cites W2078646756 @default.
- W2121525530 cites W2089362132 @default.
- W2121525530 cites W2106255922 @default.
- W2121525530 cites W2109993434 @default.
- W2121525530 cites W2111907482 @default.
- W2121525530 cites W2112372337 @default.
- W2121525530 cites W2114675972 @default.
- W2121525530 cites W2116787729 @default.
- W2121525530 cites W2117415703 @default.
- W2121525530 cites W2121780828 @default.
- W2121525530 cites W2125705042 @default.
- W2121525530 cites W2126004312 @default.
- W2121525530 cites W2128190429 @default.
- W2121525530 cites W2129239355 @default.
- W2121525530 cites W2132214317 @default.
- W2121525530 cites W2132568251 @default.
- W2121525530 cites W2134007339 @default.
- W2121525530 cites W2135601805 @default.
- W2121525530 cites W2136052329 @default.
- W2121525530 cites W2137392287 @default.
- W2121525530 cites W2138624449 @default.
- W2121525530 cites W2141231462 @default.
- W2121525530 cites W2141267333 @default.
- W2121525530 cites W2142758749 @default.
- W2121525530 cites W2144857397 @default.
- W2121525530 cites W2146625875 @default.
- W2121525530 cites W2151296838 @default.
- W2121525530 cites W2151383500 @default.
- W2121525530 cites W2153342952 @default.
- W2121525530 cites W2155192432 @default.
- W2121525530 cites W2155589041 @default.
- W2121525530 cites W2162993946 @default.
- W2121525530 cites W2164255537 @default.
- W2121525530 cites W2167121345 @default.
- W2121525530 cites W2169301387 @default.
- W2121525530 cites W2169456871 @default.
- W2121525530 cites W2170694569 @default.
- W2121525530 cites W2182272947 @default.