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Human TRAF3 adaptor molecule deficiency leads to impaired Toll-like receptor 3 response and susceptibility to herpes simplex encephalitis.

Immunity | Sep 24, 2010

Tumor necrosis factor (TNF) receptor-associated factor 3 (TRAF3) functions downstream of multiple TNF receptors and receptors that induce interferon-α (IFN-α), IFN-β, and IFN-λ production, including Toll-like receptor 3 (TLR3), which is deficient in some patients with herpes simplex virus-1 encephalitis (HSE). Mice lacking TRAF3 die in the neonatal period, preventing direct investigation of the role of TRAF3 in immune responses and host defenses in vivo. Here, we report autosomal dominant, human TRAF3 deficiency in a young adult with a history of HSE in childhood. The TRAF3 mutant allele is loss-of-expression, loss-of-function, dominant-negative and associated with impaired, but not abolished, TRAF3-dependent responses upon stimulation of both TNF receptors and receptors that induce IFN production. TRAF3 deficiency is associated with a clinical phenotype limited to HSE resulting from the impairment of TLR3-dependent induction of IFN. Thus, TLR3-mediated immunity against primary infection by HSV-1 in the central nervous system is critically dependent on TRAF3.

Pubmed ID: 20832341 RIS Download

Mesh terms: Cells, Cultured | Disease Susceptibility | Encephalitis, Herpes Simplex | Humans | Interferons | Mutation | Receptors, Tumor Necrosis Factor | TNF Receptor-Associated Factor 3 | Toll-Like Receptor 3

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Associated grants

  • Agency: NCRR NIH HHS, Id: 5UL1RR024143
  • Agency: NCRR NIH HHS, Id: UL1 RR024143-04
  • Agency: NIAID NIH HHS, Id: 1R01AI088364
  • Agency: NCRR NIH HHS, Id: UL1 RR024143
  • Agency: NIAID NIH HHS, Id: R01 AI088364
  • Agency: Howard Hughes Medical Institute, Id: R01 AI088364-01
  • Agency: NIAID NIH HHS, Id:

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