A Case for Targeting Th17 Cells and IL-17A in SARS-CoV-2 Infections.
Marika OrlovPandora L WanderEric D MorrellCarmen MikacenicMark M WurfelPublished in: Journal of immunology (Baltimore, Md. : 1950) (2020)
SARS-CoV-2, the virus causing COVID-19, has infected millions and has caused hundreds of thousands of fatalities. Risk factors for critical illness from SARS-CoV-2 infection include male gender, obesity, diabetes, and age >65. The mechanisms underlying the susceptibility to critical illness are poorly understood. Of interest, these comorbidities have previously been associated with increased signaling of Th17 cells. Th17 cells secrete IL-17A and are important for clearing extracellular pathogens, but inappropriate signaling has been linked to acute respiratory distress syndrome. Currently there are few treatment options for SARS-CoV-2 infections. This review describes evidence linking risk factors for critical illness in COVID-19 with increased Th17 cell activation and IL-17 signaling that may lead to increased likelihood for lung injury and respiratory failure. These findings provide a basis for testing the potential use of therapies directed at modulation of Th17 cells and IL-17A signaling in the treatment of COVID-19.
Keyphrases
- sars cov
- induced apoptosis
- respiratory syndrome coronavirus
- cell cycle arrest
- acute respiratory distress syndrome
- coronavirus disease
- extracorporeal membrane oxygenation
- type diabetes
- cardiovascular disease
- respiratory failure
- endoplasmic reticulum stress
- signaling pathway
- metabolic syndrome
- cell death
- oxidative stress
- body mass index
- single cell
- physical activity
- intensive care unit
- weight loss
- bone marrow
- climate change