Figure 2.

Scheme summarizing the possible involvement of dendritic cells in SARS-CoV-2 infection. Pneumocytes are infected by SARS-CoV-2 and, after pyroptosis, release viruses, PAMP (pathogen-associated molecular patterns) and DAMPS (damage-associated molecular patterns). PAMPs and DAMPs might activate dendritic cells. Moreover, DC-SIGN (localized on dendritic cells) might recognize and bind the virus. Then, dendritic cells might move toward lymph nodes. Locally, dendritic cells might affect different populations of T-lymphocytes. SARS-CoV-2 might also increase, through RAAS (renin-angiotensin-aldosterone system), the production of aldosterone (ALDO) that is intracellularly recognized by its receptor (MR) (see the text for more mechanistic details). In turn, this results in an activation of dendritic cells and macrophages. Aldosterone could also affect coagulation enhancing microthrombosis. SARS-CoV-2 also infects endothelial cells, causing hypercoagulation and affecting dendritic cells. The image also shows the cytokine storms that are due to the activation of a plethora of cells, including those of innate immunity response. In the inset, aldosterone stimulation of endothelial cells NADPH oxidases with a concomitant ROS production is shown. ROS might be also involved in the hyperinflammation condition.