Immunometabolism at the cornerstone of inflammaging, immunosenescence, and autoimmunity in COVID-19

Aging (Albany NY). 2020 Dec 27;12(24):26263-26278. doi: 10.18632/aging.202422. Epub 2020 Dec 27.

Abstract

Inflammaging constitutes the common factor for comorbidities predisposing to severe COVID-19. Inflammaging leads to T-cell senescence, and immunosenescence is linked to autoimmune manifestations in COVID-19. As in SLE, metabolic dysregulation occurs in T-cells. Targeting this T-cell dysfunction opens the field for new therapeutic strategies to prevent severe COVID-19. Immunometabolism-mediated approaches such as rapamycin, metformin and dimethyl fumarate, may optimize COVID-19 treatment of the elderly and patients at risk for severe disease.

Keywords: COVID-19; immunometabolism; immunosenescence; inflammaging; rapamycin-metformin-dimethyl fumarate.

MeSH terms

  • Autoimmunity*
  • Biomarkers
  • COVID-19 / complications
  • COVID-19 / immunology*
  • COVID-19 / metabolism*
  • COVID-19 / virology
  • Cytokine Release Syndrome / etiology
  • Cytokine Release Syndrome / prevention & control
  • Energy Metabolism*
  • Enhancer Elements, Genetic
  • Host-Pathogen Interactions*
  • Humans
  • Immunosenescence*
  • Promoter Regions, Genetic
  • SARS-CoV-2 / genetics
  • SARS-CoV-2 / immunology*
  • Signal Transduction
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Biomarkers
  • TOR Serine-Threonine Kinases