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Profound Treg perturbations correlate with COVID-19 severity.

Silvia Galván-Peña1, Juliette Leon1,2, Kaitavjeet Chowdhary1

  • 1Department of Immunology, Harvard Medical School, Boston, MA 02115.

Proceedings of the National Academy of Sciences of the United States of America
|August 26, 2021
PubMed
Summary
This summary is machine-generated.

Severe COVID-19 involves immune dysfunction. Researchers found that T regulatory cells (Tregs) with increased FoxP3 expression worsen outcomes by suppressing antiviral responses and promoting inflammation.

Keywords:
COVID-19FoxP3Tregstumor Tregs

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Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Severe COVID-19 is characterized by uncontrolled inflammation due to immune dysfunction.
  • T regulatory cells (Tregs) are crucial for maintaining immune homeostasis.

Purpose of the Study:

  • To investigate the role of FoxP3+ T regulatory cells (Tregs) in the pathology of severe COVID-19.
  • To identify specific Treg phenotypes and molecular mechanisms contributing to COVID-19 severity.

Main Methods:

  • Flow cytometry and transcriptomic profiling of immune cells from severe COVID-19 patients.
  • Analysis of Treg proportions, FoxP3 expression, and gene signatures.
  • Screening for candidate therapeutic agents affecting Treg function.

Main Results:

  • Severe COVID-19 patients exhibited an increased proportion of Tregs with elevated FoxP3 levels, correlating with poor outcomes.
  • These Tregs displayed a unique transcriptional profile, overexpressing suppressive and proinflammatory molecules (e.g., IL-32), resembling tumor-infiltrating Tregs.
  • These Treg alterations were most pronounced during acute disease but persisted into convalescence.
  • Interleukin-6 (IL-6) and Interleukin-18 (IL-18) were identified as potential contributors to these Treg perturbations.

Conclusions:

  • Tregs may play a detrimental role in severe COVID-19 by suppressing essential antiviral T cell responses.
  • Proinflammatory functions of Tregs, potentially mediated by molecules like IL-32, contribute to COVID-19 pathology.
  • Targeting specific Treg pathways could offer therapeutic strategies for severe COVID-19.