Nature Immunology, Published online: 30 June 2025; doi:10.1038/s41590-025-02213-8

FOXP3 dependence



Summary

A new study published in Nature Immunology reveals a crucial dependency on the transcription factor FOXP3 for the sustained suppressive function of regulatory T cells (Tregs). The research, conducted in a mouse model of autoimmune diabetes, demonstrates that transient depletion of FOXP3, even after initial Treg development, leads to a rapid loss of Treg identity and function. This results in the conversion of Tregs into pathogenic effector T cells, exacerbating autoimmune disease. The findings highlight the critical role of continuous FOXP3 expression in maintaining Treg stability and suggest that targeting factors influencing FOXP3 stability could be a promising therapeutic approach for autoimmune diseases.

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