A Case for Targeting Th17 Cells and IL-17A in SARS-CoV-2 Infections

J Immunol. 2020 Aug 15;205(4):892-898. doi: 10.4049/jimmunol.2000554. Epub 2020 Jul 10.

Abstract

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.

Publication types

  • Review

MeSH terms

  • Antibodies, Monoclonal, Humanized / adverse effects
  • Antibodies, Monoclonal, Humanized / therapeutic use*
  • Betacoronavirus / immunology*
  • COVID-19
  • COVID-19 Drug Treatment
  • Comorbidity
  • Coronavirus Infections / drug therapy
  • Coronavirus Infections / epidemiology*
  • Coronavirus Infections / immunology*
  • Coronavirus Infections / virology
  • Critical Illness
  • Female
  • Humans
  • Interleukin-17 / antagonists & inhibitors*
  • Interleukin-17 / metabolism
  • Male
  • Pandemics
  • Pneumonia, Viral / epidemiology*
  • Pneumonia, Viral / immunology*
  • Pneumonia, Viral / virology
  • Respiratory Distress Syndrome / immunology
  • Respiratory Distress Syndrome / mortality
  • Respiratory Distress Syndrome / virology
  • Risk Factors
  • SARS-CoV-2
  • Signal Transduction / drug effects
  • Signal Transduction / immunology
  • Th17 Cells / drug effects*
  • Th17 Cells / immunology

Substances

  • Antibodies, Monoclonal, Humanized
  • IL17A protein, human
  • Interleukin-17