title: Pathological pain and the neuroimmune interface.
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.
authors.affiliation: 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.
authors.forename: Peter M
authors.initials: PM
authors.lastname: Grace
authors.affiliation: 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.
authors.forename: Mark R
authors.initials: MR
authors.lastname: Hutchinson
authors.affiliation: Department of Psychology and Neuroscience, and The Center for Neuroscience, University of Colorado Boulder, Boulder 80309-0345, USA.
authors.forename: Steven F
authors.initials: SF
authors.lastname: Maier
authors.affiliation: Department of Psychology and Neuroscience, and The Center for Neuroscience, University of Colorado Boulder, Boulder 80309-0345, USA.
authors.forename: Linda R
authors.initials: LR
authors.lastname: Watkins
mesh_terms: D000818:Animals; D002490:Central Nervous System / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D018925:Chemokines / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D008954:Models, Biological; D015213:Neuroimmunomodulation / Q000276:immunology* / Q000502:physiology*; D010146:Pain / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology*; D059408:Pain Management; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000276:immunology
chemical_list: D018925:Chemokines; D051193:Toll-Like Receptors