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Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
T regulatory lymphocytes specific for SARS-CoV-2 display increased functional plasticity
Laura Esparcia-Pinedo1, Ángel Lancho-Sánchez1, Ilya Tsukalov2
1Immunology Department, Hospital Universitario de La Princesa and Instituto de Investigación Sanitaria Princesa, Madrid, Spain.
Immune cells called T regulatory (Treg) lymphocytes show increased CCR9 and CCR6 expression in response to SARS-CoV-2. This suggests a role for these adaptable cells in COVID-19 severity and autoimmune conditions.
Area of Science:
- Immunology
- Virology
- Pathogenesis
Background:
- Understanding immune cell roles in SARS-CoV-2 infection is crucial for COVID-19 pathogenesis and disease variability.
- Chemokine receptor expression on T lymphocytes influences immune responses and disease outcomes.
Purpose of the Study:
- To analyze chemokine receptor expression (CCR9, CCR6) on SARS-CoV-2-specific CD4+ T lymphocytes.
- To investigate the functional characteristics and heterogeneity of regulatory T cells (Tregs) in COVID-19 and vaccinated individuals.
Main Methods:
- Flow cytometry analysis of chemokine receptor expression on CD4+ T cells.
- Assessment of cytokine production (IL-10, IL-17) and transcription factor expression (FoxP3, Notch4).
- Comparison of immune cell profiles in vaccinated donors, convalescent individuals, and COVID-19 patients.
Main Results:
- Increased CCR9+ and CCR6+ CD4+ T cells were observed in vaccinated individuals and COVID-19 patients.
- CCR9+ CD4+ T cells were enriched in regulatory T cells (Tregs) with heterogeneous regulatory activity.
- CCR6+ Tregs were significantly increased in critically ill COVID-19 patients, suggesting a role in lung injury.
Conclusions:
- A SARS-CoV-2-specific Treg population exhibits increased plasticity, contributing to varied disease responses.
- This Treg plasticity may underlie differential COVID-19 pathogenesis and the development of post-infection autoimmune conditions.
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