Gene therapy directed at the neuroimmune component of chronic pain with particular attention to the role of TNF alpha.
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 TNFalpha in spinal glia in the modulation of chronic pain.
Mata
Marina
M
Department of Neurology, University of Michigan, 1914 Taubman Center, 1500 E. Medical Center Drive, Ann Arbor, MI 48109-0316, USA; VA Ann Arbor Healthcare System, Ann Arbor, MI 48109-0316, USA.
Hao
Shuanglin
S
Fink
David J
DJ
D000818:Animals; D015316:Genetic Therapy / Q000379:methods*; D006801:Humans; D007155:Immunologic Factors / Q000096:biosynthesis / Q000378:metabolism; D059408:Pain Management; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism / Q000502:physiology*
D007155:Immunologic Factors; D014409:Tumor Necrosis Factor-alpha