2020
DOI: 10.1016/j.lfs.2020.118102
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Contribution of monocytes and macrophages to the local tissue inflammation and cytokine storm in COVID-19: Lessons from SARS and MERS, and potential therapeutic interventions

Abstract: The COVID-19-, SARS-and MERS-related coronaviruses share many genomic and structural similarities. However, the SARS-CoV-2 is less pathogenic than SARS-CoV and MERS-CoV. Despite some differences in the cytokine patterns, it seems that the cytokine storm plays a crucial role in the pathogenesis of COVID-19-, SARSand MERS. Monocytes and macrophages may be infected by SARS-CoV-2 through ACE2-dependent and ACE2independent pathways. SARS-CoV-2 can effectively suppress the anti-viral IFN response in monocytes and ma… Show more

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Cited by 287 publications
(339 citation statements)
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References 119 publications
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“…During SARS-CoV-2 infections, immune cell subsets change, and among the B cells, the plasma cells increased remarkably, whereas the naïve B cells decreased [44]. Interestingly, one of the characteristics of the formation of SARS-CoV-2 anti-virus antibodies in a trial to limit viral replication is that these protective antibodies will cause friendly damage by the binding of the virus-Ab complex to FcR on monocytes/macrophages induces pro-inflammatory responses that end up with the accumulation of pro-inflammatory M1 macrophages in the lungs escalating lung injury [45].…”
Section: Hachim Et Al Translational Medicine Communicationsmentioning
confidence: 99%
“…During SARS-CoV-2 infections, immune cell subsets change, and among the B cells, the plasma cells increased remarkably, whereas the naïve B cells decreased [44]. Interestingly, one of the characteristics of the formation of SARS-CoV-2 anti-virus antibodies in a trial to limit viral replication is that these protective antibodies will cause friendly damage by the binding of the virus-Ab complex to FcR on monocytes/macrophages induces pro-inflammatory responses that end up with the accumulation of pro-inflammatory M1 macrophages in the lungs escalating lung injury [45].…”
Section: Hachim Et Al Translational Medicine Communicationsmentioning
confidence: 99%
“…First, GM-CSF was upregulated before TNF, IL-6, and MCP-1 in animal model of SARS-CoV infection 32 , and its excessive production adversely contributed to the SARS-CoV-induced lung injury 32 . Second, consistent with the critical contribution of myeloid cells to cytokine storm 28 , the percentage of GM-CSF-expressing leukocytes was significantly increased in a subset of patients with severe COVID-19 33,34 . Thus, the excessive production of GM-CSF may adversely propagate a dysregulated cytokine storm in a subset of COVID-19 patients (Fig.…”
Section: Discussionmentioning
confidence: 53%
“…Furthermore, we have found two RBM-cross-reactive monoclonal antibodies that competitively and MCP-1). It has also been suggested as a "driver" of the disease progression particularly in a subset (~ 20%) of COVID-19 patients with more severe pneumonia that often escalates to respiratory failure and death [26][27][28][29] . Furthermore, GM-CSF might also be a key mediator of the cytokine storm in COVID-19 and other inflammatory diseases 30,31 .…”
Section: Discussionmentioning
confidence: 99%
“…During SARS-CoV-2 infections, immune cell subsets change, and among the B cells, the plasma cells increased remarkably, whereas the naïve B cells decreased [45]. Interestingly, one of the characteristics of the formation of SARS-CoV-2 anti-virus antibodies in a trial to limit viral replication is that these protective antibodies will cause friendly damage by the binding of the virus-Ab complex to FcR on monocytes/macrophages induces pro-in ammatory responses that end up with the accumulation of pro-in ammatory M1 macrophages in the lungs escalating lung injury [46].…”
Section: Discussionmentioning
confidence: 99%