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TCF19 drives a broad transcriptional program that potentiates optimal innate and adaptive functions of antiviral NK cells

GSE265814 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 7 samples Submitted 2025/06/23 Platform GPL24247
Summary
Natural killer (NK) cells are innate lymphocytes that play a critical role in host defense against viral infection. In addition to rapid effector cytokine production and direct cytotoxicity, NK cells exhibit features of adaptive immunity, including the capacity to undergo robust antigen-specific clonal proliferation and to generate immunological memory. However, the transcriptional programs and regulators governing dynamic NK cell responses to viral infection have not been fully uncovered. In this study, we identified Transcription factor 19 (TCF19) as a key driver of NK cell proliferation and calcium signaling in the context of mouse cytomegalovirus infection. Ablation of TCF19 was detrimental to NK cell clonal expansion and host protection against viral infection. Tcf19-/- NK cells were also unable to properly mobilize calcium downstream of antigen signaling to mediate cytotoxicity. Altogether, we find that TCF19 drives a transcriptional program that coordinates the innate and adaptive NK cell responses against viral infection.
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TCF19 drives a broad transcriptional program that potentiates optimal innate and adaptive functions of antiviral NK cells
Dang C, Kim H, Santosa EK et al. · Nature immunology 2025 · PMID 40781555 · doi:10.1038/s41590-025-02238-z
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Direct links to NCBI, no account and no request form: the whole study as GSE265814_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 7 samples. Raw sequencing reads are also available from ENA.

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Also filed as BioProject PRJNA1104251 and SRA study SRP503900. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40781555) ↗
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