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

By K. Tabeta, P. Georgel, E. Janssen, Xin Du, K. Hoebe, K. Crozat, Suzanne Mudd, L. Shamel, Sosathya Sovath, Jason Goode and 3 more. Proceedings of the National Academy of Sciences of the United States of America, 2004

1,051 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/a4e6eb9856dc8e85ccbaac9b81e07aa9eff4c416

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Citations in the corpus

Toll-like receptors in antiviral innate immunity (2013, background): “Mutations in the receptor domain of TLR9 abolished its ability to recognize CpG oligonucleotides following MCMV infection [73].”
TLR3: interferon induction by double-stranded RNA including poly(I:C). (2008, background): “MCMV dsDNA Survival [76] Vial load in spleens ↑ IFN-α/β, IL-12 and IFN-γ in serum ↓ NK and NKT cell activation ↓ LCMV ssRNA (−) Normal CD4 or CD8 T cell responses [69]”
Innate immune recognition of viral infection (2006, background): “Accordingly, TLR3-deficient mice are susceptible to MCMV infection because of reduced interferon productio”
Anti-immunology: evasion of the host immune system by bacterial and viral pathogens. (2006, background): “For example, TLR3-mi- nus mice infected with a variety of RNA viruses undergo normal pathogenesis and immune responses (Edelmann et al., 2004; Schroder and Bowie, 2005), whereas TLR3 is critical for responses to at least one DNA virus, murine cytomegalovirus (Tabeta et al., 2004).”
Toll-like Receptor 3-mediated Necrosis via TRIF, RIP3, and MLKL* (2013, background): “Signaling fromTLR3 andTLR9 collaborate in restricting systemicMCMV infection in vivo (58).”
The Unc93b1 mutation 3d disrupts exogenous antigen presentation and signaling via Toll-like receptors 3, 7 and 9 (2006, background): “Immunodeficiency states in which TLR signaling is altered or abolished have been systematically created and identified using the random germline mutagen N -ethyl- N -nitrosoure”
Immunobiology of Human Cytomegalovirus: from Bench to Bedside (2009, background): “Exploiting Cellular Immune Responses Attempts to passively restore HCMV cellular immunity in humans were instigated following data from MCMV models in which the adoptive transfer of CD8 T cells protected against viral challenge (181, 211), together with findings that the recovery of HCMV-specific T-”