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. Author manuscript; available in PMC: 2024 Mar 25.
Published in final edited form as: Semin Respir Crit Care Med. 2023 Jan 16;44(1):100–117. doi: 10.1055/s-0042-1759778

Fig.1.

Fig.1

Immune pathogenesis of SARS-CoV-2 infection and possible therapeutic targets for the rationale of glucocorticoids employment. A type I IFN response is elicited by SARS-CoV-2 and contributes to viral clearance, leading to mild forms of the infection. In patients with a low type I IFN response, NF-kB activation predominates, culminating in the production of great amounts of inflammatory cytokines (i.e., IL-6, IL-1, and TNF-α) which in turn amplify the mechanism of NF-kB-mediated inflammation. This exuberant inflammatory response leads to hyperinflammatory syndrome, severe COVID-19, and cytokine storm. Glucocorticoids inhibit NF-kB activation, thus attenuating this harmful and dysregulated inflammatory response (Dashed arrows stand for inhibition). COVID-19, coronavirus disease 2019; IFN, interferons; IL, interleukin; MAS, macropahge activating syndrome; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2.