Fig. 1.

Possible mechanism of cytokine release syndrome in severe coronavirus disease 2019 (COVID-19) patients. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects alveolar epithelial cells [mainly alveolar epithelial type 2 (AEC2) cells] through the angiotensin-converting enzyme 2 (ACE2) receptor. Destruction of epithelial cells and the increase of cell permeability lead to release of the virus. SARS-CoV-2 activates the innate immune system; macrophages and other innate immune cells not only capture the virus but also release a large number of cytokines and chemokines, including interleukin-6 (IL-6). Adaptive immunity is also activated by antigen-presenting cells (mainly dendritic cells). T- and B-cells not only play an antiviral role but also directly or indirectly promote the secretion of inflammatory cytokines. In addition, under the stimulation of inflammatory factors, a large number of inflammatory exudates and erythrocytes enter the alveoli, resulting in dyspnoea and respiratory failure.