Journal
CELLS
Volume 9, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/cells9102290
Keywords
TNFR1; TNFR2; TNF therapy; demyelination; neurodegeneration; synaptic damage; experimental autoimmune encephalomyelitis; cuprizone; Theiler’ s murine encephalomyelitis virus
Categories
Funding
- FISM grant (Fondazione Italiana Sclerosi Multipla) [2019/S/1]
- '5 per mille' public fund
- Italian Ministry of Universities and Research (MIUR-PRIN) [2017K55HLC]
- Italian Ministry of Health [GR-2016-02361163, GR-2016-02362380, GR-2018-12366154, RF-2018-12366144]
- Ricerca corrente to IRCCS San Raffaele Pisana
- Ricerca corrente and '5 per mille' public fund
- FISM-Fondazione Italiana Sclerosi Multipla [2018/B/2]
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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.
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