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Glia. 2016 Apr;64(4):475-86. doi: 10.1002/glia.22899. Epub 2015 Aug 6.

Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies?

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Department of Neurology, Developmental Neurobiology, University Hospital Würzburg, Würzburg, D-97080, Germany.
Institute of Infection, Immunity and Inflammation College of Medical Veterinary and Life Sciences, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow, G12 8TA.


The role of innate and adaptive inflammation as a primary driver or modifier of neuropathy in premorbidly normal nerves, and as a critical player in amplifying neuropathies of other known causes (e.g., genetic, metabolic) is incompletely understood and under-researched, despite unmet clinical need. Also, cellular and humoral components of the adaptive and innate immune system are substantial disease modifying agents in the context of neuropathies and, at least in some neuropathies, there is an identified tight interrelationship between both compartments of the immune system. Additionally, the quadruple relationship between Schwann cell, axon, macrophage, and endoneurial fibroblast, with their diverse membrane bound and soluble signalling systems, forms a distinct focus for investigation in nerve diseases with inflammation secondary to Schwann cell mutations and possibly others. Identification of key immunological effector pathways that amplify neuropathic features and associated clinical symptomatology including pain should lead to realistic and timely possibilities for translatable therapeutic interventions using existing immunomodulators, alongside the development of novel therapeutic targets.


adaptive immune system; fibroblast; innate immune system; lymphocytes; macrophage; nodes of Ranvier

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