FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2012373229> ?p ?o ?g. }

• W2012373229 endingPage "e1003637" @default.
• W2012373229 startingPage "e1003637" @default.
• W2012373229 abstract "Herpes simplex encephalitis (HSE) is a lethal neurological disease resulting from infection with Herpes Simplex Virus 1 (HSV-1). Loss-of-function mutations in the UNC93B1, TLR3, TRIF, TRAF3, and TBK1 genes have been associated with a human genetic predisposition to HSE, demonstrating the UNC93B-TLR3-type I IFN pathway as critical in protective immunity to HSV-1. However, the TLR3, UNC93B1, and TRIF mutations exhibit incomplete penetrance and represent only a minority of HSE cases, perhaps reflecting the effects of additional host genetic factors. In order to identify new host genes, proteins and signaling pathways involved in HSV-1 and HSE susceptibility, we have implemented the first genome-wide mutagenesis screen in an in vivo HSV-1 infectious model. One pedigree (named P43) segregated a susceptible trait with a fully penetrant phenotype. Genetic mapping and whole exome sequencing led to the identification of the causative nonsense mutation L3X in the Receptor-type tyrosine-protein phosphatase C gene (PtprcL3X), which encodes for the tyrosine phosphatase CD45. Expression of MCP1, IL-6, MMP3, MMP8, and the ICP4 viral gene were significantly increased in the brain stems of infected PtprcL3X mice accounting for hyper-inflammation and pathological damages caused by viral replication. PtprcL3X mutation drastically affects the early stages of thymocytes development but also the final stage of B cell maturation. Transfer of total splenocytes from heterozygous littermates into PtprcL3X mice resulted in a complete HSV-1 protective effect. Furthermore, T cells were the only cell population to fully restore resistance to HSV-1 in the mutants, an effect that required both the CD4+ and CD8+ T cells and could be attributed to function of CD4+ T helper 1 (Th1) cells in CD8+ T cell recruitment to the site of infection. Altogether, these results revealed the CD45-mediated T cell function as potentially critical for infection and viral spread to the brain, and also for subsequent HSE development." @default.
• W2012373229 created "2016-06-24" @default.
• W2012373229 creator A5007863049 @default.
• W2012373229 creator A5009682091 @default.
• W2012373229 creator A5014245073 @default.
• W2012373229 creator A5015907831 @default.
• W2012373229 creator A5017363021 @default.
• W2012373229 creator A5021307048 @default.
• W2012373229 creator A5024481569 @default.
• W2012373229 creator A5025353152 @default.
• W2012373229 creator A5026168352 @default.
• W2012373229 creator A5038553084 @default.
• W2012373229 creator A5040878528 @default.
• W2012373229 creator A5049725885 @default.
• W2012373229 creator A5057060810 @default.
• W2012373229 creator A5058671714 @default.
• W2012373229 creator A5065027577 @default.
• W2012373229 creator A5067397938 @default.
• W2012373229 creator A5074877667 @default.
• W2012373229 creator A5083756296 @default.
• W2012373229 date "2013-09-12" @default.
• W2012373229 modified "2023-10-13" @default.
• W2012373229 title "Genome-Wide Mouse Mutagenesis Reveals CD45-Mediated T Cell Function as Critical in Protective Immunity to HSV-1" @default.
• W2012373229 cites W1509718831 @default.
• W2012373229 cites W1520347430 @default.
• W2012373229 cites W1539667460 @default.
• W2012373229 cites W1567207438 @default.
• W2012373229 cites W1608729016 @default.
• W2012373229 cites W1656644461 @default.
• W2012373229 cites W1942267505 @default.
• W2012373229 cites W1944135917 @default.
• W2012373229 cites W1964452168 @default.
• W2012373229 cites W1968099474 @default.
• W2012373229 cites W1973150035 @default.
• W2012373229 cites W1973540902 @default.
• W2012373229 cites W1975264017 @default.
• W2012373229 cites W1984068087 @default.
• W2012373229 cites W1985339853 @default.
• W2012373229 cites W1987410025 @default.
• W2012373229 cites W1988551550 @default.
• W2012373229 cites W1991412053 @default.
• W2012373229 cites W1994453856 @default.
• W2012373229 cites W1995146839 @default.
• W2012373229 cites W1995796039 @default.
• W2012373229 cites W1996767948 @default.
• W2012373229 cites W1996828685 @default.
• W2012373229 cites W2001904356 @default.
• W2012373229 cites W2002229146 @default.
• W2012373229 cites W2008938292 @default.
• W2012373229 cites W2011678998 @default.
• W2012373229 cites W2014529814 @default.
• W2012373229 cites W2017284605 @default.
• W2012373229 cites W2021490494 @default.
• W2012373229 cites W2021750859 @default.
• W2012373229 cites W2027228821 @default.
• W2012373229 cites W2032634316 @default.
• W2012373229 cites W2033193447 @default.
• W2012373229 cites W2033441782 @default.
• W2012373229 cites W2033828724 @default.
• W2012373229 cites W2034651748 @default.
• W2012373229 cites W2037951817 @default.
• W2012373229 cites W2039120803 @default.
• W2012373229 cites W2041216249 @default.
• W2012373229 cites W2043687376 @default.
• W2012373229 cites W2046899821 @default.
• W2012373229 cites W2050193841 @default.
• W2012373229 cites W2050204298 @default.
• W2012373229 cites W2050242791 @default.
• W2012373229 cites W2051956916 @default.
• W2012373229 cites W2053159643 @default.
• W2012373229 cites W2053611532 @default.
• W2012373229 cites W2055743270 @default.
• W2012373229 cites W2056107229 @default.
• W2012373229 cites W2056650797 @default.
• W2012373229 cites W2059013205 @default.
• W2012373229 cites W2060029228 @default.
• W2012373229 cites W2074986753 @default.
• W2012373229 cites W2077083557 @default.
• W2012373229 cites W2080136687 @default.
• W2012373229 cites W2084603524 @default.
• W2012373229 cites W2086478422 @default.
• W2012373229 cites W2092628933 @default.
• W2012373229 cites W2097550991 @default.
• W2012373229 cites W2099480987 @default.
• W2012373229 cites W2102619694 @default.
• W2012373229 cites W2103441770 @default.
• W2012373229 cites W2105233670 @default.
• W2012373229 cites W2108182701 @default.
• W2012373229 cites W2108234281 @default.
• W2012373229 cites W2114876320 @default.
• W2012373229 cites W2116883279 @default.
• W2012373229 cites W2121070193 @default.
• W2012373229 cites W2122801955 @default.
• W2012373229 cites W2123586959 @default.
• W2012373229 cites W2130909829 @default.
• W2012373229 cites W2131606729 @default.
• W2012373229 cites W2131718269 @default.
• W2012373229 cites W2131987313 @default.

• next