Antiviral type I interferons (IFN) produced in the early phase of viral infections
effectively inhibit viral replication, prevent virus-mediated tissue damages and promote
innate and adaptive immune responses that are all essential to the successful elimination
of viruses. As professional type I IFN producing cells, plasmacytoid dendritic cells
(pDC) have the ability to rapidly produce waste amounts of type I IFNs. Therefore,
their low frequency, dysfunction or decreased capacity to produce type I IFNs might
increase the risk of severe viral infections. In accordance with that, declined pDC
numbers and delayed or inadequate type I IFN responses could be observed in patients
with severe coronavirus disease (COVID-19) caused by the severe acute respiratory
syndrome coronavirus 2 (SARS-CoV-2), as compared to individuals with mild or no symptoms.
Thus, besides chronic diseases, all those conditions, which negatively affect the
antiviral IFN responses lengthen the list of risk factors for severe COVID-19. In
the current review, we would like to briefly discuss the role and dysregulation of
pDC/type I IFN axis in COVID-19, and introduce those type I IFN-dependent factors,
which account for an increased risk of COVID-19 severity and thus are responsible
for the different magnitude of individual immune responses to SARS-CoV-2.
