Akal Taşcıoğlu, DidemAkkaya, EmreGenc, Sema2021-05-282021-05-282021Tascioglu, D., Akkaya, E., & Genc, S. (2021). The understanding of the immunopathology in COVID-19 infection. Scandinavian journal of clinical and laboratory investigation, 1–9. Advance online publication. https://doi.org/10.1080/00365513.2021.18928170036-55131502-7686https://doi.org/10.1080/00365513.2021.1892817https://hdl.handle.net/20.500.12713/1763Coronaviruses belonging to the Coronaviridae family are single-stranded RNA viruses. The entry of SARS-CoV-2 is accomplished via ACE-2 receptors. SARS-CoV-2 infection coactivates both innate and adaptive immune responses. Although SARS-CoV-2 stimulates antibody production with a typical pattern of IgM/IgG, cellular immunity is also impaired. In severe cases, low CD4 + and CD8 + T cell counts are associated with impaired immune functions, and high neutrophil/lymphocyte ratios accompanying low lymphocyte subsets have been demonstrated. Recently, high IFN -?/? ratios with impaired T cell responses, and increased IL-1, IL-6, TNF-?, MCP-1, IP-10, IL-4, IL-10 have been reported in COVID-19 infection. Increased proinflammatory cytokines and chemokines in patients with severe COVID-19 may cause the suppression of CD4 + and CD8 + T cells and regulatory T cells, causing excessive inflammatory responses and fatal cytokine storm with tissue and organ damage. Consequently, novel therapeutics to be developed against host immune system, including blockade of cytokines (IL-6, IL-1, IFN) themselves, their receptors or signaling pathways- JAK inhibitors- could be effective as potential therapeutics.eninfo:eu-repo/semantics/closedAccessCOVID-19ChemokinesCytokinesImmunotherapyPandemicsThe understanding of the immunopathology in COVID-19 infectionArticle1934032527WOS:0006540518000012-s2.0-85106524178Q410.1080/00365513.2021.1892817Q2