The Role of Th17 Response in COVID-19.
Diana MartonikAnna Parfieniuk-KowerdaMagdalena RogalskaRobert FlisiakPublished in: Cells (2021)
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)-1β, 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.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- coronavirus disease
- immune response
- induced apoptosis
- randomized controlled trial
- signaling pathway
- end stage renal disease
- cell cycle arrest
- chronic kidney disease
- toll like receptor
- oxidative stress
- newly diagnosed
- cell death
- endothelial cells
- inflammatory response
- cell proliferation
- quantum dots
- drinking water
- prognostic factors
- cerebrospinal fluid