ArticleJournal of translational autoimmunity2025
Targeted regulatory T cell activation by site-specific PEGylated interleukin-2 mitigates autoimmune inflammation.
Article in Journal of translational autoimmunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Dysregulation of immune homeostasis accompanied by regulatory T cell (Treg) dysfunction is a hallmark of various autoimmune and inflammatory diseases. While low-dose interleukin-2 (IL-2) treatment can enhance Treg levels and alleviate disease symptoms, its short half-life necessitates frequent dosing. Furthermore, adverse events associated with the activation of other immune cells are often observed. In this study, using a site-specific PEGylation approach, we developed a novel IL-2 variant, I129-W80, which exhibited an IL-2Rα-biased binding profile, driven by the steric hindrance of the PEG moiety. It selectively activated Tregs in vitro and could overcome inhibition by the endogenous decoy receptor, soluble IL-2Rα, unlike the Fc-fusion IL-2 variant AMG-592. In a single-dose monkey study, I129-W80 demonstrated an extended half-life, along with sustained amplification and activation of Tregs. At the maximum dose that did not induce C-reactive protein elevation, I129-W80 showed superior activity compared with AMG-592. I129-W80 improved inflammatory responses in both delayed-type hypersensitivity and xenogeneic graft-versus-host disease models. Additionally, in an imiquimod-induced dermatitis model, I129-W80 exhibited reduced distribution to inflamed tissues compared with AMG-592. These findings demonstrated that I129-W80 possesses distinct properties relative to Fc-fusion IL-2 variant and can correct immune imbalances caused by Treg dysfunction, thereby improving the symptoms of various autoimmune diseases.
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