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@ARTICLE{Vicua:127706,
      author       = {L. Vicuña and D. E. Strochlic and A. Latremoliere and K.
                      K. Bali and M. Simonetti and D. Husainie and S. Prokosch$^*$
                      and P. Riva and R. S. Griffin and C. Njoo and S. Gehrig and
                      M. A. Mall and B. Arnold$^*$ and M. Devor and C. J. Woolf
                      and S. D. Liberles and M. Costigan and R. Kuner},
      title        = {{T}he serine protease inhibitor {S}erpin{A}3{N} attenuates
                      neuropathic pain by inhibiting {T} cell-derived leukocyte
                      elastase.},
      journal      = {Nature medicine},
      volume       = {21},
      number       = {5},
      issn         = {1546-170X},
      address      = {New York, NY},
      publisher    = {Nature America Inc.},
      reportid     = {DKFZ-2017-03729},
      pages        = {518 - 523},
      year         = {2015},
      abstract     = {Neuropathic pain is a major, intractable clinical problem
                      and its pathophysiology is not well understood. Although
                      recent gene expression profiling studies have enabled the
                      identification of novel targets for pain therapy, classical
                      study designs provide unclear results owing to the
                      differential expression of hundreds of genes across sham and
                      nerve-injured groups, which can be difficult to validate,
                      particularly with respect to the specificity of pain
                      modulation. To circumvent this, we used two outbred lines of
                      rats, which are genetically similar except for being
                      genetically segregated as a result of selective breeding for
                      differences in neuropathic pain hypersensitivity. SerpinA3N,
                      a serine protease inhibitor, was upregulated in the dorsal
                      root ganglia (DRG) after nerve injury, which was further
                      validated for its mouse homolog. Mice lacking SerpinA3N
                      developed more neuropathic mechanical allodynia than
                      wild-type (WT) mice, and exogenous delivery of SerpinA3N
                      attenuated mechanical allodynia in WT mice. T lymphocytes
                      infiltrate the DRG after nerve injury and release leukocyte
                      elastase (LE), which was inhibited by SerpinA3N derived from
                      DRG neurons. Genetic loss of LE or exogenous application of
                      a LE inhibitor (Sivelastat) in WT mice attenuated
                      neuropathic mechanical allodynia. Overall, we reveal a novel
                      and clinically relevant role for a member of the serpin
                      superfamily and a leukocyte elastase and crosstalk between
                      neurons and T cells in the modulation of neuropathic pain.},
      keywords     = {Acute-Phase Proteins (NLM Chemicals) / Enzyme Inhibitors
                      (NLM Chemicals) / Serpina3n protein, mouse (NLM Chemicals) /
                      Serpina3n protein, rat (NLM Chemicals) / Serpins (NLM
                      Chemicals) / Leukocyte Elastase (NLM Chemicals)},
      cin          = {D050},
      ddc          = {610},
      cid          = {I:(DE-He78)D050-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25915831},
      pmc          = {pmc:PMC4450999},
      doi          = {10.1038/nm.3852},
      url          = {https://inrepo02.dkfz.de/record/127706},
}