TLR3 deficiency in patients with herpes simplex encephalitis.

Détails

ID Serval
serval:BIB_ED3AFF47EDB9
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
TLR3 deficiency in patients with herpes simplex encephalitis.
Périodique
Science
Auteur⸱e⸱s
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.
ISSN
1095-9203[electronic]
Statut éditorial
Publié
Date de publication
2007
Volume
317
Numéro
5844
Pages
1522-1527
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
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.
Mots-clé
Alleles, CD8-Positive T-Lymphocytes/immunology, Cell Line, Child, Preschool, Dendritic Cells/immunology, Encephalitis, Herpes Simplex/genetics, Encephalitis, Herpes Simplex/immunology, Female, Fibroblasts/immunology, Fibroblasts/metabolism, Genes, Dominant, Herpesvirus 1, Human/physiology, Heterozygote, Humans, Immunity, Innate, Infant, Interferons/biosynthesis, Keratinocytes/immunology, Killer Cells, Natural/immunology, Leukocytes, Mononuclear/immunology, Mutation, Poly I-C/pharmacology, Toll-Like Receptor 3/chemistry, Toll-Like Receptor 3/deficiency
Pubmed
Web of science
Création de la notice
28/01/2008 12:27
Dernière modification de la notice
20/08/2019 17:15
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