PMID- 37483590
OWN - NLM
STAT- MEDLINE
DCOM- 20230725
LR  - 20231106
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 14
DP  - 2023
TI  - Role of tumor necrosis factor-alpha in the central nervous system: a focus on 
      autoimmune disorders.
PG  - 1213448
LID - 10.3389/fimmu.2023.1213448 [doi]
LID - 1213448
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a pleiotropic immune cytokine that belongs 
      to the TNF superfamily of receptor ligands. The cytokine exists as either a 
      transmembrane or a soluble molecule, and targets two distinct receptors, TNF-alpha 
      receptor 1 (TNFR1) and TNF-alpha receptor 2 (TNFR2), which activate different 
      signaling cascades and downstream genes. TNF-alpha cellular responses depend on its 
      molecular form, targeted receptor, and concentration levels. TNF-alpha plays a 
      multifaceted role in normal physiology that is highly relevant to human health 
      and disease. In the central nervous system (CNS), this cytokine regulates 
      homeostatic functions, such as neurogenesis, myelination, blood-brain barrier 
      permeability and synaptic plasticity. However, it can also potentiate neuronal 
      excitotoxicity and CNS inflammation. The pleiotropism of TNF-alpha and its various 
      roles in the CNS, whether homeostatic or deleterious, only emphasizes the 
      functional complexity of this cytokine. Anti-TNF-alpha therapy has demonstrated 
      effectiveness in treating various autoimmune inflammatory diseases and has 
      emerged as a significant treatment option for CNS autoimmune diseases. 
      Nevertheless, it is crucial to recognize that the effects of this therapeutic 
      target are diverse and complex. Contrary to initial expectations, anti-TNF-alpha 
      therapy has been found to have detrimental effects in multiple sclerosis. This 
      article focuses on describing the various roles, both physiological and 
      pathological, of TNF-alpha in the CNS. Additionally, it discusses the specific 
      disease processes that are dependent or regulated by TNF-alpha and the rationale of 
      its use as a therapeutic target.
CI  - Copyright (c) 2023 Gonzalez Caldito.
FAU - Gonzalez Caldito, Natalia
AU  - Gonzalez Caldito N
AD  - Department of Neurology, Northwestern Memorial Hospital, Feinberg School of 
      Medicine, Northwestern University, Chicago, IL, United States.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20230707
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Tumor Necrosis Factor Inhibitors)
RN  - 0 (Cytokines)
SB  - IM
MH  - Humans
MH  - *Tumor Necrosis Factor-alpha
MH  - Tumor Necrosis Factor Inhibitors
MH  - Central Nervous System
MH  - Cytokines
MH  - *Multiple Sclerosis
PMC - PMC10360935
OTO - NOTNLM
OT  - Neuro-Behcet's disease
OT  - TNF-a
OT  - central nervous system
OT  - cytokines
OT  - microglia
OT  - multiple sclerosis
OT  - neuroinflammation
OT  - neurosarcoidosis
COIS- The author declares that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2023/07/24 06:42
MHDA- 2023/07/25 06:42
PMCR- 2023/01/01
CRDT- 2023/07/24 04:32
PHST- 2023/04/28 00:00 [received]
PHST- 2023/06/14 00:00 [accepted]
PHST- 2023/07/25 06:42 [medline]
PHST- 2023/07/24 06:42 [pubmed]
PHST- 2023/07/24 04:32 [entrez]
PHST- 2023/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2023.1213448 [doi]
PST - epublish
SO  - Front Immunol. 2023 Jul 7;14:1213448. doi: 10.3389/fimmu.2023.1213448. 
      eCollection 2023.