eEF2K Enhances Virus-Specific Effector CD8+ T Cell Responses During Viral Infection 2314

Abstract Description Eukaryotic Elongation Factor-2 Kinase (eEF2K), a well-known negative regulator of protein synthesis, has been extensively studied in cancer biology, yet its role in immune cells, particularly T cells, remains underexplored. In this study, we investigated eEF2K’s impact on T cells during vaccinia virus (VACV) infection. Our results demonstrate that eEF2K-deficient (eEF2K-/-) mice exhibit an increased proportion of VACV-specific effector CD8+ T cells without compromising the formation of VACV-specific memory T cells. RNA-sequencing analysis further revealed that eEF2K-/- VACV-specific effector CD8+ T cells possess enhanced functionality, improving their effectiveness in combating viral infection during the effector stage. Notably, we identified TRAF3 as a key mediator of the amplified antiviral response observed in eEF2K-/- VACV-specific effector CD8+ T cells. These findings suggest that targeting eEF2K may be a promising approach to boost effector CD8+ T cell responses during viral infections. Funding Sources Supported by NIH R01CA221867 and R21AI167793. Topic Categories Immune Response Regulation: Molecular Mechanisms (IRM)

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Publication Details

Journal
The Journal of Immunology
Published
2025-11-01
DOI
https://doi.org/10.1093/jimmun/vkaf283.243
Primary Topic
Cancer Immunotherapy and Biomarkers
Type
article
Field-Weighted Citation Impact
0.00

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article

eEF2K Enhances Virus-Specific Effector CD8+ T Cell Responses During Viral Infection 2314

Jinyoung Song, Liqing Wang, Xiaofang Xiong
The Journal of Immunology
Cancer Immunotherapy and Biomarkers
article

eEF2K Enhances Virus-Specific Effector CD8+ T Cell Responses During Viral Infection 2314

Jinyoung Song, Liqing Wang, Xiaofang Xiong
article en

Abstract

Abstract Description Eukaryotic Elongation Factor-2 Kinase (eEF2K), a well-known negative regulator of protein synthesis, has been extensively studied in cancer biology, yet its role in immune cells, particularly T cells, remains underexplored. In this study, we investigated eEF2K’s impact on T cells during vaccinia virus (VACV) infection. Our results demonstrate that eEF2K-deficient (eEF2K-/-) mice exhibit an increased proportion of VACV-specific effector CD8+ T cells without compromising the formation of VACV-specific memory T cells. RNA-sequencing analysis further revealed that eEF2K-/- VACV-specific effector CD8+ T cells possess enhanced functionality, improving their effectiveness in combating viral infection during the effector stage. Notably, we identified TRAF3 as a key mediator of the amplified antiviral response observed in eEF2K-/- VACV-specific effector CD8+ T cells. These findings suggest that targeting eEF2K may be a promising approach to boost effector CD8+ T cell responses during viral infections. Funding Sources Supported by NIH R01CA221867 and R21AI167793. Topic Categories Immune Response Regulation: Molecular Mechanisms (IRM)

The Journal of ImmunologyVol. 214(Supplement_1)
Texas A&M University (US)
Cancer Research Institute, State Key Laboratory of Pharmaceutical Biotechnology, National Institutes of Health
Openalex Percentile: Top 51%
Cancer Immunotherapy and Biomarkers
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