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Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies?
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....
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4832258/ https://www.ncbi.nlm.nih.gov/pubmed/26250643 http://dx.doi.org/10.1002/glia.22899 |
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author | Martini, Rudolf Willison, Hugh |
author_facet | Martini, Rudolf Willison, Hugh |
author_sort | Martini, Rudolf |
collection | PubMed |
description | 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 |
format | Online Article Text |
id | pubmed-4832258 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-48322582016-04-20 Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies? Martini, Rudolf Willison, Hugh Glia Review Articles 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 John Wiley and Sons Inc. 2015-08-06 2016-04 /pmc/articles/PMC4832258/ /pubmed/26250643 http://dx.doi.org/10.1002/glia.22899 Text en © 2015 The Authors. Glia Published by Wiley Periodicals, Inc. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Articles Martini, Rudolf Willison, Hugh Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies? |
title | Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies? |
title_full | Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies? |
title_fullStr | Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies? |
title_full_unstemmed | Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies? |
title_short | Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies? |
title_sort | neuroinflammation in the peripheral nerve: cause, modulator, or bystander in peripheral neuropathies? |
topic | Review Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4832258/ https://www.ncbi.nlm.nih.gov/pubmed/26250643 http://dx.doi.org/10.1002/glia.22899 |
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