Gene therapy directed at the neuroimmune component of chronic pain with particular attention to the role of TNFα

Marina Mata, Shuanglin Hao, David J. Fink

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Identification that neuroimmune activation in the spinal cord is an important factor in the development of chronic pain has opened the possibility that gene transfer of anti-inflammatory peptides may be used to reduce pain neurotransmission. We review the published evidence regarding gene transfer to meninges to express the anti-inflammatory peptide interleukin 10, and gene transfer to dorsal root ganglia using replication incompetent HSV vectors to express interleukin 4, interleukin 10, or the soluble (p55) tumor necrosis factor receptor (sTNFR). The results of these experiments suggest a novel role for "reverse signaling" through the full-length membrane form of TNFα in spinal glia in the modulation of chronic pain.

Original languageEnglish (US)
Pages (from-to)209-213
Number of pages5
JournalNeuroscience Letters
Volume437
Issue number3
DOIs
StatePublished - Jun 6 2008

Keywords

  • Cytokines
  • Gene therapy
  • Gene transfer
  • Herpes simplex virus
  • Neuropathic pain
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Neuroscience(all)

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