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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.
Summary
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.
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.
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