eEF-2K Deficiency Boosts the Virus-Specific Effector CD8<sup>+</sup> T Cell Responses During Viral Infection
In this study, we revealed a critical role of eukaryotic elongation factor-2 kinase (eEF-2K), a negative regulator of protein synthesis, in regulating T cells during vaccinia virus (VACV) infection. We found that eEF-2K-deficient (eEF-2K⁻/⁻) mice exhibited a significantly higher proportion of VACV-s...
Saved in:
| Main Authors: | , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2024-12-01
|
| Series: | Viruses |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1999-4915/17/1/26 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Summary: | In this study, we revealed a critical role of eukaryotic elongation factor-2 kinase (eEF-2K), a negative regulator of protein synthesis, in regulating T cells during vaccinia virus (VACV) infection. We found that eEF-2K-deficient (eEF-2K⁻/⁻) mice exhibited a significantly higher proportion of VACV-specific effector CD8<sup>+</sup> T cells without compromising the development of VACV-specific memory CD8<sup>+</sup> T cells. RNA sequencing demonstrated that eEF-2K⁻/⁻ VACV-specific effector CD8<sup>+</sup> T cells had enhanced functionality, which improves their capacity to combat viral infection during the effector phase. Moreover, we identified tumor necrosis factor receptor-associated factor 3 (TRAF3) as a critical mediator of the stronger antiviral response observed in eEF-2K⁻/⁻ effector CD8<sup>+</sup> T cells. These findings suggest that targeting eEF-2K may provide a novel strategy to augmenting effector CD8<sup>+</sup> T cell responses against viral infections. |
|---|---|
| ISSN: | 1999-4915 |