The role of the immune system in the generation of neuropathic pain

Margarita Calvo; John M. Dawes; David L. H. Bennett

doi:10.1016/S1474-4422(12)70134-5

The role of the immune system in the generation of neuropathic pain

Margarita Calvo, John M. Dawes, David L. H. Bennett

King's College London

Research output: Contribution to journal › Literature review › peer-review

371 Citations (Scopus)

Abstract

Persistent pain is a sequela of several neurological conditions with a primary immune basis, such as Guillain-Barre syndrome and multiple sclerosis. Additionally, diverse forms of injury to the peripheral or the central nervous systems-whether traumatic, metabolic, or toxic-result in substantial recruitment and activation of immune cells. This response involves the innate immune system, but evidence also exists of T-lymphocyte recruitment, and in some patient cohorts antibodies to neuronal antigens have been reported. Mediators released by immune cells, such as cytokines, sensitise nociceptive signalling in the peripheral and central nervous systems. Preclinical data suggest an immune pathogenesis of neuropathic pain, but clinical evidence of a central role of the immune system is less clear. An important challenge for the future is to establish to what extent this immune response initiates or maintains neuropathic pain in patients and thus whether it is amenable to therapy.

Original language	English
Pages (from-to)	629-642
Number of pages	14
Journal	Lancet Neurology
Volume	11
Issue number	7
DOIs	https://doi.org/10.1016/S1474-4422(12)70134-5
Publication status	Published - Jul 2012

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title = "The role of the immune system in the generation of neuropathic pain",

abstract = "Persistent pain is a sequela of several neurological conditions with a primary immune basis, such as Guillain-Barre syndrome and multiple sclerosis. Additionally, diverse forms of injury to the peripheral or the central nervous systems-whether traumatic, metabolic, or toxic-result in substantial recruitment and activation of immune cells. This response involves the innate immune system, but evidence also exists of T-lymphocyte recruitment, and in some patient cohorts antibodies to neuronal antigens have been reported. Mediators released by immune cells, such as cytokines, sensitise nociceptive signalling in the peripheral and central nervous systems. Preclinical data suggest an immune pathogenesis of neuropathic pain, but clinical evidence of a central role of the immune system is less clear. An important challenge for the future is to establish to what extent this immune response initiates or maintains neuropathic pain in patients and thus whether it is amenable to therapy.",

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AU - Calvo, Margarita

AU - Dawes, John M.

AU - Bennett, David L. H.

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N2 - Persistent pain is a sequela of several neurological conditions with a primary immune basis, such as Guillain-Barre syndrome and multiple sclerosis. Additionally, diverse forms of injury to the peripheral or the central nervous systems-whether traumatic, metabolic, or toxic-result in substantial recruitment and activation of immune cells. This response involves the innate immune system, but evidence also exists of T-lymphocyte recruitment, and in some patient cohorts antibodies to neuronal antigens have been reported. Mediators released by immune cells, such as cytokines, sensitise nociceptive signalling in the peripheral and central nervous systems. Preclinical data suggest an immune pathogenesis of neuropathic pain, but clinical evidence of a central role of the immune system is less clear. An important challenge for the future is to establish to what extent this immune response initiates or maintains neuropathic pain in patients and thus whether it is amenable to therapy.

AB - Persistent pain is a sequela of several neurological conditions with a primary immune basis, such as Guillain-Barre syndrome and multiple sclerosis. Additionally, diverse forms of injury to the peripheral or the central nervous systems-whether traumatic, metabolic, or toxic-result in substantial recruitment and activation of immune cells. This response involves the innate immune system, but evidence also exists of T-lymphocyte recruitment, and in some patient cohorts antibodies to neuronal antigens have been reported. Mediators released by immune cells, such as cytokines, sensitise nociceptive signalling in the peripheral and central nervous systems. Preclinical data suggest an immune pathogenesis of neuropathic pain, but clinical evidence of a central role of the immune system is less clear. An important challenge for the future is to establish to what extent this immune response initiates or maintains neuropathic pain in patients and thus whether it is amenable to therapy.

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DO - 10.1016/S1474-4422(12)70134-5

M3 - Literature review

SN - 1474-4422

VL - 11

SP - 629

EP - 642

JO - Lancet Neurology

JF - Lancet Neurology

IS - 7

ER -

The role of the immune system in the generation of neuropathic pain

Abstract

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