Endothelial cell, myeloid, and adaptive immune responses in SARS-CoV-2 infection

SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) is an emerging respiratory pathogen that has rapidly spread in human populations. Severe forms of infection associate cytokine release syndrome and acute lung injury due to hyperinflammatory responses even though virus clearance is achieved. Key components of inflammation include immune cell recruitment in infected tissues, a step which is under the control of endothelial cells. Here, we review endothelial cell responses in inflammation and infection due to SARS-CoV-2 together with phenotypic and functional alterations of monocytes, T and B lymphocytes with which they interact. We surmise that endothelial cells function as an integrative and active platform for the various cells recruited, where fine tuning of immune responses takes place and which provides opportunities for therapeutic intervention.

Automated summary

In the inflammation and infection caused by SARS-CoV-2, endothelial cells play a crucial role in regulating the recruitment of immune cells and interacting with monocytes, T cells, and B cells. Endothelial cells function as an integrative and active platform for immune responses, providing opportunities for therapeutic intervention.