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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
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CD85k Contributes to Regulatory T Cell Function in Chronic Viral Infections
Anna Estrada Brull1, Felix Rost1, Josua Oderbolz2
1Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland.
International Journal of Molecular Sciences
|December 30, 2020
Summary
Regulatory T cells (Tregs) specialize during chronic viral infections. Type 1 Tregs use CD85k to suppress Th1 cells, revealing a new mechanism for controlling persistent immune responses.
Area of Science:
- Immunology
- Cellular Biology
- Virology
Background:
- Regulatory T cells (Tregs) are crucial for immune homeostasis and preventing pathology during infections.
- Tregs exhibit functional specialization into distinct subsets to adapt to various immune environments.
- The specialization of Tregs during chronic infections remains poorly understood.
Purpose of the Study:
- To investigate Treg specialization in persistent viral infections.
- To identify mechanisms of Treg-mediated immune suppression during chronic viral infections.
Main Methods:
- Utilized lymphocytic choriomeningitis virus (LCMV) and murine cytomegalovirus (MCMV) infection models.
- Investigated the expression and function of CD85k and its ligand ALCAM on T cells.
- Assessed Treg-mediated suppression of Th1 effector cells.
Main Results:
- Identified CD85k as a Th1-specific co-inhibitory receptor with sustained expression in persistent viral infections.
- Demonstrated that recombinant CD85k inhibits effector T cells.
- Showed induced expression of ALCAM on exhausted T cells during chronic LCMV infection.
- Type 1 Tregs in chronic LCMV infection suppress Th1 cells via an ALCAM-dependent mechanism.
Conclusions:
- Treg specialization extends from acute to persistent viral infections.
- CD85k plays a significant role in Treg-mediated suppression of type 1 immunity during chronic viral infections.
- Revealed a novel ALCAM-dependent pathway for Treg-mediated immune control.
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