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      Pathological pain and the neuroimmune interface

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          Abstract

          Reciprocal signalling between immunocompetent cells in the central nervous system (CNS) has emerged as a key phenomenon underpinning pathological and chronic pain mechanisms. Neuronal excitability can be powerfully enhanced both by classical neurotransmitters derived from neurons, and by immune mediators released from CNS-resident microglia and astrocytes, and from infiltrating cells such as T cells. In this Review, we discuss the current understanding of the contribution of central immune mechanisms to pathological pain, and how the heterogeneous immune functions of different cells in the CNS could be harnessed to develop new therapeutics for pain control. Given the prevalence of chronic pain and the incomplete efficacy of current drugs — which focus on suppressing aberrant neuronal activity — new strategies to manipulate neuroimmune pain transmission hold considerable promise.

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          Author and article information

          Journal
          101124169
          27017
          Nat Rev Immunol
          Nat. Rev. Immunol.
          Nature reviews. Immunology
          1474-1733
          1474-1741
          24 May 2017
          28 February 2014
          April 2014
          25 July 2017
          : 14
          : 4
          : 217-231
          Affiliations
          [1 ]Department of Psychology and Neuroscience, and The Center for Neuroscience, University of Colorado Boulder, Boulder 80309–0345, USA
          [2 ]School of Medical Sciences, University of Adelaide, Adelaide 5005, Australia
          Author notes
          Correspondence to P.M.G. peter.grace@ 123456colorado.edu
          Article
          PMC5525062 PMC5525062 5525062 nihpa877853
          10.1038/nri3621
          5525062
          24577438
          Categories
          Article

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