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The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

TLR3 Deficiency in Patients with Herpes Simplex Encephalitis

Zhang, Shen-Ying, Jouanguy, Emmanuelle, Ugolini, Sophie, Smahi, Asma, Elain, Gaëlle, Romero, Pedro, Segal, David, Sancho-Shimizu, Vanessa, Lorenzo, Lazaro, Puel, Anne, Picard, Capucine, Chapgier, Ariane, Plancoulaine, Sabine, Titeux, Matthias, Cognet, Céline, von Bernuth, Horst, Ku, Cheng-Lung, Casrouge, Armanda, Zhang, Xin-Xin, Barreiro, Luis, Leonard, Joshua, Hamilton, Claire, Lebon, Pierre, Héron, Bénédicte, Vallée, Louis, Quintana-Murci, Lluis, Hovnanian, Alain, Rozenberg, Flore, Vivier, Eric, Geissmann, Frédéric, Tardieu, Marc, Abel, Laurent, Casanova, Jean-Laurent·2007·Science
DOI 10.1126/science.1139522
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Abstract

Some Toll and Toll-like receptors (TLRs) provide immunity to experimental infections in animal models, but their contribution to host defense in natural ecosystems is unknown. We report a dominant-negative TLR3 allele in otherwise healthy children with herpes simplex virus 1 (HSV-1) encephalitis. TLR3 is expressed in the central nervous system (CNS), where it is required to control HSV-1, which spreads from the epithelium to the CNS via cranial nerves. TLR3 is also expressed in epithelial and dendritic cells, which apparently use TLR3-independent pathways to prevent further dissemination of HSV-1 and to provide resistance to other pathogens in TLR3-deficient patients. Human TLR3 appears to be redundant in host defense to most microbes but is vital for natural immunity to HSV-1 in the CNS, which suggests that neurotropic viruses have contributed to the evolutionary maintenance of TLR3.

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Crossref · 10.1126/science.1139522

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2 of 2 references verified0 citation errors · 0 not checkable

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  • An increased risk of herpes encephalitis after HSV-1 infection is observed in children with autosomal dominant mutations in TLR3, indicating that TLR3 trafficking by UNC93B1 is crucial for the control of HSV-1 infection.

    “Consistent with this, an increased risk of herpes encephalitis after HSV-1 infection is observed in children with autosomal dominant mutations in TLR3, indicating that TLR3 trafficking by UNC93B1 is crucial for the control of HSV-1 infection (50).”

    From UNC93B1 Is Widely Expressed in the Murine CNS and Is Required for Neuroinflammation and Neuronal Injury Induced by MicroRNA let-7b (2021) · cites this paper as [50]

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Metadata

Authors
Zhang, S.-Y., Jouanguy, E., Ugolini, S., Smahi, A., Elain, G., Romero, P., Segal, D., Sancho-Shimizu, V., Lorenzo, L., Puel, A., Picard, C., Chapgier, A., Plancoulaine, S., Titeux, M., Cognet, C., von Bernuth, H., Ku, C.-L., Casrouge, A., Zhang, X.-X., Barreiro, L., Leonard, J., Hamilton, C., Lebon, P., Héron, B., Vallée, L., Quintana-Murci, L., Hovnanian, A., Rozenberg, F., Vivier, E., Geissmann, F., Tardieu, M., Abel, L., & Casanova, J.-L.
Affiliations
Human Genetics of Infectious Diseases, Institut National de la Santé et de la Recherche Médicale (INSERM), U550, Faculty Necker, Paris 75015, France.
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
2007-09-14
Volume
317
Issue
5844
Pages
1522-1527
ISSN
  • 0036-8075
  • 1095-9203
DOI
10.1126/science.1139522
Cited by
1,057
References
2
Language
en

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