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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
Regulatory T cells in virus infections
Barry T Rouse1, Pranita P Sarangi, Susmit Suvas
1Department of Microbiology, The University of Tennessee, Knoxville, TN 37996, USA.
Immunological Reviews
|August 15, 2006
Summary
Regulatory T cells (Tregs) can limit or aid viral immune responses. Understanding Treg influence is key to controlling viral infections and immunopathology.
Area of Science:
- Immunology
- Virology
Background:
- Regulatory T cells (Tregs), specifically CD4+ CD25+ forkhead box protein 3+ natural Tregs (nTregs), significantly influence immune responses during viral infections.
- The role of Tregs in viral infections is complex, with potential to both impair and protect the host.
Purpose of the Study:
- To review the dual role of Tregs in modulating immune responses to viral infections.
- To explore how Tregs impact viral control, persistence, and immunopathology.
- To discuss potential therapeutic strategies targeting Tregs for viral diseases.
Main Methods:
- This review synthesizes existing in vitro and in vivo data on Treg function during viral infections.
- It examines specific examples including herpes simplex virus (HSV), hepatitis C virus (HCV), and human immunodeficiency virus (HIV).
Main Results:
- Normal nTreg function can limit the magnitude and efficacy of antiviral immune responses, as seen with HSV, where nTreg depletion enhances viral control.
- Treg responses can contribute to immune dysfunction and viral persistence (e.g., HCV, HIV) by promoting chronic tissue damage.
- Conversely, nTregs can be protective by limiting immunopathology, such as in HSV-induced eye lesions and by mitigating chronic immune activation in HIV.
Conclusions:
- Tregs present a double-edged sword in viral infections, necessitating a nuanced understanding for therapeutic intervention.
- Manipulating Treg responses holds potential for enhancing antiviral immunity or reducing virus-induced tissue damage.
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