TLR3 deficiency in patients with herpes simplex encephalitis

Science. 2007 Sep 14;317(5844):1522-7. doi: 10.1126/science.1139522.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 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
  • Fibroblasts / virology
  • 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*
  • Toll-Like Receptor 3 / genetics*
  • Toll-Like Receptor 3 / physiology

Substances

  • TLR3 protein, human
  • Toll-Like Receptor 3
  • Interferons
  • Poly I-C