NDLI: Toll-like receptors 9 and 3 as essential components of innate immune defense against mouse cytomegalovirus infection

Content Provider	PubMed Central
Author	Tabeta, Koichi Philippe, Georgel Janssen, Edith Du, Xin Kasper, Hoebe Crozat, Karine Mudd, Suzanne Shamel, Louis Sovath, Sosathya Goode, Jason Alexopoulou, Lena Flavell, Richard A. Beutler, Bruce
Copyright Year	2004
Abstract	Several subsets of dendritic cells have been shown to produce type I IFN in response to viral infections, thereby assisting the natural killer cell-dependent response that eliminates the pathogen. Type I IFN production can be induced both by unmethylated CpG-oligodeoxynucleotide and by double-stranded RNA. Here, we describe a codominant CpG-ODN unresponsive phenotype that results from an N-ethyl-N-nitrosourea-induced missense mutation in the Tlr9 gene (Tlr9CpG1 ). Mice homozygous for the Tlr9CpG1 allele are highly susceptible to mouse cytomegalovirus infection and show impaired infection-induced secretion of IFN-α/β and natural killer cell activation. We also demonstrate that both the Toll-like receptor (TLR) 9 → MyD88 and TLR3 → Trif signaling pathways are activated in vivo on viral inoculation, and that each pathway contributes to innate defense against systemic viral infection. Whereas both pathways lead to type I IFN production, neither pathway offers full protection against mouse cytomegalovirus infection in the absence of the other. The Tlr9CpG1 mutation alters a leucine-rich repeat motif and lies within a receptor domain that is conserved within the evolutionary cluster encompassing TLRs 7, 8, and 9. In other TLRs, including three mouse-specific TLRs described in this paper, the affected region is not represented. The phenotypic effect of the Tlr9CpG1 allele thus points to a critical role for TLR9 in viral sensing and identifies a vulnerable amino acid within the ectodomain of three TLR proteins, essential for a ligand response.
Related Links	http://dx.doi.org/10.1073/pnas.0400525101
Ending Page	3521
Page Count	6
Starting Page	3516
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	10
Volume Number	101
Language	English
Publisher	National Academy of Sciences
Publisher Date	2004-03-09
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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