PMC:7543426 / 23680-24778 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7543426","sourcedb":"PMC","sourceid":"7543426","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7543426","text":"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 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