TY  - JOUR
A1  - Martini, Rudolf
A1  - Willison, Hugh
T1  - Neuroinflammation in the peripheral nerve: cause, modulator, or bystander in peripheral neuropathies?
JF  - GLIA
N2  - 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.
KW  - Charcot-Marie-Tooth
KW  - Guillain-Barré-Syndrom
KW  - familial amyloidotic polyneuropathy
KW  - motor axonal neuropathy
KW  - Schwann cell dedifferentiation
KW  - glycation end products
KW  - innate immune system
KW  - adaptive immune system
KW  - macrophage
KW  - fibroblast
KW  - lymphocytes
KW  - nodes of Ranvier
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-189696
VL  - 64
IS  - 4
ER  -