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Yes. Platelets are those cells that in turn activate endothelium. There is a billion of these platelets and megakaryocytes PARKED in the lung microvascular space. https://www.biorxiv.org/content/10.1101/2020.11.08.372581v1
And there is an overabundance of evidence that SARS-CoV-2 significantly activates platelets beyond what is seen typically in ARDS of other etiologies.
There is probably a dysregulated milieu with dysregulated serotonin and other mediators that drive the dysregulated B cell response, leading to afucosylated Ig development that essentially puts the disease in the next gear with autoimmunity that further activates platelets, etc.
Afucosylated Ig against variety of intrinsic molecules also develops in another platelet-opathy
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3901064/
How platelet activation leads to a milieu change in fucosylation is worth studying in COVID19.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3901064/
How platelet activation leads to a milieu change in fucosylation is worth studying in COVID19.
Whether dysregulated serotonin leads to a pro-fibrotic and dysregulated immune response is not a new concept, it’s been shown in at least one other disease process: https://www.nature.com/articles/s41598-017-15348-y
And in lung fibrosis https://thorax.bmj.com/content/65/11/949
How this platelet activation and its mediators release affects humoral response is not quite clear ...
Here is a recent review: https://www.frontiersin.org/articles/10.3389/fimmu.2020.00186/full
Here is a recent review: https://www.frontiersin.org/articles/10.3389/fimmu.2020.00186/full
