Clinical studies have indicated that acute respiratory distress syndrome and multiple organ failure are features of severe cases of COVID-19. These are thought to be underpinned by an excessive immune response [19]. In the lung microenvironment, excessive inflammatory cytokine may be caused by immune-pathological changes linked to lymphocytic infiltration. We demonstrated a significant upregulation of the chemokine receptor CXCR3, which is not only responsible for T cells extravasating from blood vessels and migration [20], but it has been also implicated in pulmonary fibrosis [21]. It is thus possible that this is associated with an aberrant type I immune response involving the CXCR3/ligand pathway. In addition, we found intense expression of CD26/DPP4, a protein that plays a key role in T-cell signal transduction processes as a costimulatory molecule, and its expression level is known to correlate with the severity of inflammation [22]. Thus, the CXCR3 cytokine axis could be considered a potential therapeutic target in development of targeted host-directed therapies for COVID-19.