Fig. 2　Mechanisms underlying COVID-19 severity.

SARS-CoV-2 infects the lung blood vessels, leading to exudative vasculitis (left). This damage recruits non-canonical monocytes that produce thrombospondin-1 (THBS-1) and promote platelet activation. Activated platelets release MYL9, which is deposited in thrombi, and its serum levels are correlated with the disease severity (left). Reportedly, 10% of severe COVID-19 patients have autoantibodies (auto-abs) against type I interferon (IFN) (right). These auto-abs can inhibit the binding of IFN-a to its receptor, leading to impaired IFN signaling.