Re-Examining the Role of TNF in MS Pathogenesis and Therapy.
TNF therapy
TNFR1
TNFR2
Theiler’s murine encephalomyelitis virus
cuprizone
demyelination
experimental autoimmune encephalomyelitis
neurodegeneration
synaptic damage
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
14 10 2020
14 10 2020
Historique:
received:
21
09
2020
revised:
10
10
2020
accepted:
12
10
2020
entrez:
17
10
2020
pubmed:
18
10
2020
medline:
7
4
2021
Statut:
epublish
Résumé
Multiple sclerosis (MS) is a common neurological disorder of putative autoimmune origin. Clinical and experimental studies delineate abnormal expression of specific cytokines over the course of the disease. One major cytokine that has been shown to play a pivotal role in MS is tumor necrosis factor (TNF). TNF is a pleiotropic cytokine regulating many physiological and pathological functions of both the immune system and the central nervous system (CNS). Convincing evidence from studies in human and experimental MS have demonstrated the involvement of TNF in various pathological hallmarks of MS, including immune dysregulation, demyelination, synaptopathy and neuroinflammation. However, due to the complexity of TNF signaling, which includes two-ligands (soluble and transmembrane TNF) and two receptors, namely TNF receptor type-1 (TNFR1) and type-2 (TNFR2), and due to its cell- and context-differential expression, targeting the TNF system in MS is an ongoing challenge. This review summarizes the evidence on the pathophysiological role of TNF in MS and in different MS animal models, with a special focus on pharmacological treatment aimed at controlling the dysregulated TNF signaling in this neurological disorder.
Identifiants
pubmed: 33066433
pii: cells9102290
doi: 10.3390/cells9102290
pmc: PMC7602209
pii:
doi:
Substances chimiques
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
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