Journal
INTERNATIONAL REVIEWS OF IMMUNOLOGY
Volume 41, Issue 2, Pages 217-230Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/08830185.2021.1884248
Keywords
COVID-19; cytokine release syndrome; IL-6; hemophagocytic lymphohistiocytosis (HLH); Kawasaki disease; multisystem inflammatory syndrome in children (MIS-C); NF-κ B; SARS-CoV-2
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Funding
- Beijing Municipal Natural Science Foundation General Program [7192197]
- National Key Research and Development Program [2018YFC2002400, 2020YFC2002700]
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COVID-19, triggered by SARS-CoV-2, can lead to severe cases with cytokine release syndrome (CRS) and cytokine storm. IL-6 plays a crucial role in the severity of the disease and is a potential target for treatment.
The coronavirus disease 2019 (COVID-19) triggered by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) erupted in Hubei Province of China in December 2019 and has become a pandemic. Severe COVID-19 patients who suffer from acute respiratory distress syndrome (ARDS) and multi-organ dysfunction have high mortality. Several studies have shown that this is closely related to the cytokine release syndrome (CRS), often loosely referred to as cytokine storm. IL-6 is one of the key factors and its level is positively correlated with the severity of the disease. The molecular mechanisms for CRS in COVID-19 are related to the effects of the S-protein and N-protein of the virus and its ability to trigger NF-kappa B activation by disabling the inhibitory component I kappa B. This leads to activation of immune cells and the secretion of proinflammatory cytokines such as IL-6 and TNF-alpha. Other mechanisms related to IL-6 include its interaction with GM-CSF and interferon responses. The pivotal role of IL-6 makes it a target for therapeutic agents and studies on tocilizumab are already ongoing. Other possible targets of treating CRS in COVID-19 include IL-1 beta and TNF-alpha. Recently, reports of a CRS like illness called multisystem inflammatory syndrome in children (MIS-C) in children have surfaced, with a variable presentation which in some cases resembles Kawasaki disease. It is likely that the immunological derangement and cytokine release occurring in COVID-19 cases is variable, or on a spectrum, that can potentially be governed by genetic factors. Currently, there are no approved biological modulators for the treatment of COVID-19, but the urgency of the pandemic has led to numerous clinical trials worldwide. Ultimately, there is great promise that an anti-inflammatory modulator targeting a cytokine storm effect may prove to be very beneficial in reducing morbidity and mortality in COVID-19 patients.
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