ArticleiScience2024
Interleukin-2 receptor signaling acts as a checkpoint that influences the distribution of regulatory T cell subsets.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- IL-2/CD25 acts within the tumor microenvironment to reprogram tumor-specific cytotoxic CD8Journal for immunotherapy of cancer · 2026Article
- The transcription factor SREBP2 supports the activation and homeostasis of CD4+ Foxp3+ regulatory T cells.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Skeletal muscle dysfunction induced by cancer immunotherapy: mechanistics insights and surgical implications.Frontiers in immunology · 2026Review
- IgE, anti-IgE therapy, and regulatory T cells: new paradigms in allergic inflammation.Frontiers in allergy · 2026Review
- Article
- Dynamics and variegation in the Treg response to Interleukin-2.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Induction of high numbers of TBMC immunology · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Regulatory T cells (Tregs) require IL-2 for survival in the periphery, yet how IL-2 shapes Treg heterogeneity remains poorly defined. Here we show that inhibition of IL-2R signaling in post-thymic Tregs leads to a preferential early loss of circulating Tregs (cTregs). Gene expression of cTregs was more dependent on IL-2R signaling than effector Tregs (eTregs). Unexpectedly, ablation of IL-2R signaling in cTregs resulted in increased proliferation, expression of eTreg genes, and enhanced capacity to develop into eTregs. Thus, IL-2R signaling normally acts as a checkpoint to maintain cTreg homeostasis while restraining their development into eTregs. Loss of IL-2R signaling also alters the distribution of eTreg subsets, with increased IFNγR1
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.