One of the hallmarks of COVID-19 is the cytokine storm that provokes
primarily pneumonia followed by systemic inflammation. Emerging evidence
has identified a potential link between elevated levels of
interleukin-17A (IL-17A) and disease severity and progression.
Considering that per se IL-17A can activate several inflammatory
pathways, it is plausible to hypothesize an involvement of this cytokine
in COVID-19 clinical outcomes. Thus, this cytokine can represent a
marker of disease progression and/or a target to develop therapeutic
strategies. This hypothesis paper aims to propose this “unique”
cytokine as a silent amplifier of the COVID-19 immune response and
(potentially) related therapy.