TLR3 deficiency in patients with herpes simplex encephalitis.
Details
Serval ID
serval:BIB_ED3AFF47EDB9
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
TLR3 deficiency in patients with herpes simplex encephalitis.
Journal
Science
ISSN
1095-9203[electronic]
Publication state
Published
Issued date
2007
Volume
317
Number
5844
Pages
1522-1527
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
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.
Keywords
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
Create date
28/01/2008 12:27
Last modification date
20/08/2019 17:15