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10.3390/cells10061550

http://scihub22266oqcxt.onion/10.3390/cells10061550
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34205262!8235311!34205262
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suck abstract from ncbi

pmid34205262      Cells 2021 ; 10 (6): ä
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  • The Role of Th17 Response in COVID-19 #MMPMID34205262
  • Martonik D; Parfieniuk-Kowerda A; Rogalska M; Flisiak R
  • Cells 2021[Jun]; 10 (6): ä PMID34205262show ga
  • COVID-19 is an acute infectious disease of the respiratory system caused by infection with the SARS-CoV-2 virus (Severe Acute Respiratory Syndrome Coronavirus 2). Transmission of SARS-CoV-2 infections occurs through droplets and contaminated objects. A rapid and well-coordinated immune system response is the first line of defense in a viral infection. However, a disturbed and over-activated immune response may be counterproductive, causing damage to the body. Severely ill patients hospitalised with COVID-19 exhibit increased levels of many cytokines, including Interleukin (IL)-1beta, IL-2, IL-6, IL-7, IL-8, IL-10, IL-17, granulocyte colony stimulating factor (G-CSF), monocyte chemoattractant protein 1 (MCP-1) and tumor necrosis factor (TNF). Increasing evidence suggests that Th17 cells play an important role in the pathogenesis of COVID-19, not only by activating cytokine cascade but also by inducing Th2 responses, inhibiting Th1 differentiation and suppressing Treg cells. This review focuses on a Th17 pathway in the course of the immune response in COVID-19, and explores plausible targets for therapeutic intervention.
  • |COVID-19/*immunology/pathology/therapy[MESH]
  • |Cytokines/metabolism[MESH]
  • |Humans[MESH]
  • |Immunity, Cellular/*physiology[MESH]
  • |Immunotherapy, Adoptive/methods[MESH]
  • |SARS-CoV-2/immunology[MESH]


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