Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies?. Issue 4 (6th August 2015)
- Record Type:
- Journal Article
- Title:
- Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies?. Issue 4 (6th August 2015)
- Main Title:
- Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies?
- Authors:
- Martini, Rudolf
Willison, Hugh - Abstract:
- Abstract : 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. GLIA 2016;64:475–486 Main points: We discuss the primary inflammatory neuropathies and others in which inflammation results from genetic or metabolic abnormalities. Targeting inflammation with immune modulators may present therapeutic opportunities for currentlyAbstract : 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. GLIA 2016;64:475–486 Main points: We discuss the primary inflammatory neuropathies and others in which inflammation results from genetic or metabolic abnormalities. Targeting inflammation with immune modulators may present therapeutic opportunities for currently untreatable diseases. … (more)
- Is Part Of:
- Glia. Volume 64:Issue 4(2016:Apr.)
- Journal:
- Glia
- Issue:
- Volume 64:Issue 4(2016:Apr.)
- Issue Display:
- Volume 64, Issue 4 (2016)
- Year:
- 2016
- Volume:
- 64
- Issue:
- 4
- Issue Sort Value:
- 2016-0064-0004-0000
- Page Start:
- 475
- Page End:
- 486
- Publication Date:
- 2015-08-06
- Subjects:
- innate immune system -- adaptive immune system -- macrophage -- fibroblast -- lymphocytes -- nodes of Ranvier
Neuroglia -- Periodicals
Neurology -- Periodicals
611.0188 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1098-1136 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1002/glia.22899 ↗
- Languages:
- English
- ISSNs:
- 0894-1491
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4195.208000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 2387.xml