Figure 1.

Innate immune response mechanisms during SARS-CoV-2 infection. Innate immunity serves as the primary defense against SARS-CoV-2. When infected with SARS-CoV-2, the innate immune cells, including macrophages, neutrophils, dendritic cells (DCs), and plasmacytoid dendritic cells (pDCs), produce various pro-inflammatory cytokines and chemokines, contributing to the elimination of the infected cells. However, as a result of extensive cytokine release by the immune cells, neutrophil activation and degranulation as well as NETosis, a process where neutrophils expel their DNA to trap pathogens, could be observed. The cascade of signaling pathways involving toll-like receptor 3 (TLR3), toll-like receptor 7 (TLR7), mitochondrial antiviral-signaling protein (MAVS), and the transcription factors nuclear factor-kappa B (NF-κB) and interferon regulatory factors (IRFs) could be activated and further amplify the response, producing type I and type III interferons and other inflammatory cytokines, leading to exacerbated tissue damage. The innate immune response exhibits a multifaceted nature, including both protective and pathological outcomes in the context of COVID-19. (Created with BioRender.com).