Figure 1. The hyperactive immune response in SARS-CoV-2 infection and druggable immunologic targets in COVID-19. The SARS-CoV-2 enters the infected person via the respiratory tract and attaches to the ACE2 receptors in type-2 alveolar cells of the lungs. It subsequently activates the retinoic acid inducible gene-(RIG) I-like receptors (RLRs), which play an essential role in the activation of antiviral immune responses. Together with the intrinsic response to the viral particles, they induce hyperactive inflammatory response, marked by the activation of proinflammatory cytokines-releasing cells. Several immunologic targets were identified to have an important role in the COVID-mediated cytokine release syndrome / cytokine storm, therefore some pharmacological agents are repurposed to reduce the COVID-induced hyperinflammation and possibly also prevent the viral entry and replications. (ACE2 = angiotensin converting enzyme type-2; CoV = coronavirus; IFN = interferon; IL = interleukin; JAK = janus kinase; SARS = severe acute respiratory syndrome; NK = natural killer; STAT = signal transducer and activator of transcription; TCR = T-cell receptor; TLR = toll-like receptor; TNF = tumour necrosis factor)