Abstract |
Coronavirus disease (COVID-19) reached pandemic proportions at the beginning of 2020 and continues to be a worldwide concern. End organ damage and acute respiratory distress syndrome are the leading causes of death in severely or critically ill patients. The elevated cytokine levels in severe patients in comparison with mildly affected patients suggest that cytokine release syndrome (CRS) occurs in the severe form of the disease. In this paper, the significant role of pro-inflammatory cytokines, including IL-1, IL-6, and TNF-alpha, and their mechanism of action in the CRS cascade is explained. Potential therapeutic approaches involving anti-IL-6 and anti- TNF-alpha antibodies to fight COVID-19 and reduce mortality rate in severe cases are also discussed.
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Authors | Negar Moradian, Mahdi Gouravani, Mohammad Amin Salehi, Arash Heidari, Melika Shafeghat, Michael R Hamblin, Nima Rezaei |
Journal | European cytokine network
(Eur Cytokine Netw)
Vol. 31
Issue 3
Pg. 81-93
(Sep 01 2020)
ISSN: 1952-4005 [Electronic] France |
PMID | 33361013
(Publication Type: Journal Article, Review)
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Chemical References |
- Antibodies
- IL6 protein, human
- Interleukin-6
- Tumor Necrosis Factor-alpha
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Topics |
- Antibodies
(therapeutic use)
- COVID-19
(blood, complications, mortality)
- Cytokine Release Syndrome
(blood, drug therapy, etiology, mortality)
- Humans
- Interleukin-6
(antagonists & inhibitors, blood)
- Pandemics
- SARS-CoV-2
(metabolism)
- Tumor Necrosis Factor-alpha
(antagonists & inhibitors, blood)
- COVID-19 Drug Treatment
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