GEO series

Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells (RNA-Seq)

GSE271414 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2025/07/01 Platform GPL24247

Summary

Ripk1 plays an important role as a regulator of programmed cell death processes such as apoptosis and necroptosis, and is involved in the initiation of pro-inflammatory NF-kB signaling. Immune tolerance depends on the proper function and homeostasis of regulatory T cells. Here, we show that Treg-specific ablation of Ripk1 in mice leads to a reduction of Treg cells and spontaneous systemic autoimmunity. Using chimeric mice that allowed us to study Treg cells in the absence of inflammatory conditions, we observed a disadvantage of Ripk1-deficient compared to Ripk1-proficient Treg cells. Importantly, we did not observe impaired viability of the Ripk1-deficient Treg cells. Furthermore, single-cell RNA sequencing revealed that Ripk1 is required for the maintenance of the Treg cell transcriptional signature, which is essential for the suppressive function of Treg cells. Together, these findings highlight the fundamental role of Ripk1 in maintaining immune homeostasis by preserving the suppressive phenotype of Treg cells

Published in

Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells

Plaza-Sirvent C, Sturm H, Nocke MK et al. · Cell death and differentiation 2026 · PMID 40691281 · doi:10.1038/s41418-025-01550-3

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Also filed as BioProject PRJNA1131362 and SRA study SRP517851. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40691281) ↗

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