ArticleNature communications2025
Expression of an interleukin-2 partial agonist enhances regulatory T cell persistence and efficacy in mouse autoimmune models.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Receptor-tethered orthogonal IL-2 enhances regulatory T cell therapy.The Journal of experimental medicine · 2026Article
- T cell-targeted immunotherapies for multiple sclerosis: molecular mechanisms to therapeutic perspectives from Traditional Chinese medicine.Acta pharmacologica Sinica · 2026Article
- Thirty years in, regulatory T cells are ready for medicine.Frontiers in immunology · 2026Review
- CD8 regulatory T cell therapy in transplantation: a new path to clinical success?Transplant international : official journal of the European Society for Organ Transplantation · 2026Article
- Miniaturized IL-2/anti-IL-2 immunocytokines selectively activate and support theFrontiers in immunology · 2026Article
- Targeting intratumoral bacteria reverses MHC-I suppression and enhances nano-based chemoimmunotherapy in colorectal cancer.Military Medical Research · 2026Article
- T cell receptor associated transmembrane adaptor 1 (TRAT1) modulates human Th17 and Treg responses via PI3-kinase and STAT dependent mechanisms.Cell communication and signaling : CCS · 2025Article
- Targeting immune cell migration as therapy for inflammatory disease: a review.Frontiers in immunology · 2025Review
- The 2025 Nobel Prize in Physiology or Medicine Honors the Immune Peacekeepers.Transplant international : official journal of the European Society for Organ Transplantation · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulatory T (Treg)-based cell therapy holds promise for autoimmune and inflammatory diseases, yet challenges remain regarding the functional stability and persistence of transferred Tregs. Here we engineer Tregs to express a partial agonist form of IL-2 (IL-2pa) to enhance persistence while avoiding toxicity from excessive signaling. Mouse Tregs expressing wild-type IL-2 (Tregs-IL2wt) have only a transient growth advantage, limited by toxicity from likely excessive signaling. By contrast, mouse Tregs-IL2pa exhibit sustained expansion, long-term survival in immunocompetent mice for over a year, and bystander expansion of endogenous Tregs. Tregs-IL2pa maintain a stable activated phenotype, Treg-specific demethylation, and a diverse TCR repertoire. In vivo, prophylactic transfer of Tregs-IL2pa ameliorates multi-organ autoimmunity in a Treg depletion-induced mouse autoimmune model. Lastly, compared with control Treg, human Tregs-IL2pa show enhanced survival in the IL-2-depleted environment of immune-deficient mice and improved control of xenogeneic graft-versus-host disease. Our results thus show that IL-2pa self-sufficiency enhances the stability, durability and efficacy of Treg therapies in preclinical settings.
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