Nature Immunology, Published online: 25 July 2025; doi:10.1038/s41590-025-02244-1

Adoptive T cell therapies show limited efficacy against solid tumors owing to T cell exhaustion within the tumor microenvironment. A study now reveals that dysregulated translation, rather than transcriptional changes alone, drives T cell dysfunction by creating mitochondrial imbalance through selective protein synthesis.



Summary

Adoptive T cell therapies struggle against solid tumors due to T cell exhaustion within the tumor microenvironment. This new research in Nature Immunology pinpoints dysregulated translation, not just transcription, as a key driver of this T cell dysfunction. Specifically, the study demonstrates that imbalances in mitochondrial function arise because of selective protein synthesis driven by this dysregulated translation. This suggests targeting the translational machinery within exhausted T cells could offer a novel approach to improve the effectiveness of T cell therapies against solid tumors.

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