The understanding of the immunopathology in COVID-19 infection.


Tascioglu D., Akkaya E., Genc S.

Scandinavian journal of clinical and laboratory investigation, cilt.81, ss.255-263, 2021 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 81
  • Basım Tarihi: 2021
  • Doi Numarası: 10.1080/00365513.2021.1892817
  • Dergi Adı: Scandinavian journal of clinical and laboratory investigation
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, CINAHL, EMBASE, MEDLINE
  • Sayfa Sayıları: ss.255-263
  • Anahtar Kelimeler: COVID-19, cytokines, chemokines, immunotherapy, pandemics, ACUTE RESPIRATORY SYNDROME, MACROPHAGE ACTIVATION SYNDROME, ANGIOTENSIN-CONVERTING ENZYME, SARS-ASSOCIATED CORONAVIRUS, CYTOKINE STORM, INTERFERON, SARS-COV-2, PNEUMONIA, COV, IDENTIFICATION
  • İstanbul Üniversitesi Adresli: Evet

Özet

Coronaviruses 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 -alpha/gamma ratios with impaired T cell responses, and increased IL-1, IL-6, TNF-alpha, 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.