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FURIN regulates cytotoxic T-lymphocyte effector function and memory cell transition in mice.
Markus J T Ojanen1, Fernanda Munoz Caro1, Saara Aittomäki1
1Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
European Journal of Immunology
|April 4, 2023
Summary
The proprotein convertase subtilisin/kexin (PCSK) enzyme FURIN enhances host antiviral responses by regulating CD8+ T cell activation and function. Deleting FURIN in T cells restricts viral load and boosts interferon gamma (IFNG) production during infection.
Area of Science:
- Immunology
- Molecular Biology
- Virology
Background:
- Proprotein convertase subtilisin/kexins (PCSKs) are enzymes crucial for protein maturation.
- FURIN, a key PCSK, processes viral proteins and influences immune responses.
- The specific role of FURIN in CD8+ cytotoxic T lymphocytes (CTLs) was previously unclear.
Purpose of the Study:
- To investigate the function of FURIN in T-cell mediated immunity against viral infections.
- To elucidate the role of FURIN in CD8+ CTL activation, effector functions, and memory development.
Main Methods:
- Utilized a T-cell-specific FURIN knockout (KO) mouse model.
- Analyzed host response to lymphocytic choriomeningitis virus (LCMV) infection.
- Characterized Furin KO CD8+ T cells ex vivo, including cytokine-stimulated cells.
Main Results:
- T-cell-specific FURIN deletion restricted viral burden and increased interferon gamma (IFNG) production during LCMV infection.
- Furin KO CD8+ T cells exhibited an activated phenotype with upregulated effector genes.
- FURIN was found to regulate IL2, TNF, GZMB, TGFBR signaling, Eomes, Foxo1, Bcl6, ITGAE, and CD62L expression in activated CTLs.
Conclusions:
- T-cell expressed FURIN is essential for effective host response to viral infections.
- FURIN plays a critical role in CD8+ CTL homeostasis, activation, and memory formation.
- These findings highlight FURIN as a potential therapeutic target in viral diseases.
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