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Pathological pain and the neuroimmune interface
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Journal Article
Pathological pain and the neuroimmune interface
2014
Overview
Key Points
Local and recruited immunocompetent cells (such as microglia, astrocytes, endothelial cells, perivascular macrophages and T cells) in the central nervous system (CNS) detect neurotransmitters, chemokines and endogenous danger signals that are released by lesioned or diseased sensory neurons.
Immunocompetent cells in the central nervous system subsequently release cytokines, chemokines, prostaglandins, neurotrophic factors and reactive oxygen species that dysregulate synaptic transmission leading to amplification of nociceptive signalling.
Other facets of the immune response to neuronal lesion and disease are gaining recognition, including the necessity of pro-inflammatory mediators for repair, and regulation of pro-inflammatory responses by anti-inflammatory mediators.
Hence, the most successful treatment approaches targeting the immune system will probably integrate basic science understanding of nuanced immune responses.
Despite there being only indirect evidence for a CNS immune component to chronic pain in humans, immune-targeted therapies are showing early signs of success in treating such pain.
Here, the authors describe the immune mechanisms that are involved in pain, one of the key features of inflammation. They explain how the immune and nervous systems interact to initiate and propagate pain, and discuss the immune components that can be targeted for alleviating pathological pain in patients.
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group
