ArticleJournal of virology2026
Simultaneous TCR and IL-2 agonism selectively enhances epitope-specific CD8 T-cell responses during chronic viral infection.
Article in Journal of virology, 2026. 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
Interleukin-2 (IL-2) remains an attractive cytokine for enhancing antigen-specific CD8 T-cell responses in cancer immunotherapy, but systemic toxicity hinders its broad clinical application. To address this, various IL-2-based therapeutics have been engineered with altered IL-2 receptor bias or targeted delivery to tumors, the tumor microenvironment, or immune cell populations. Ideally, IL-2 signals should be selectively delivered to antigen-specific CD8 T cells, boosting their responses and promoting effector differentiation while sparing non-targeted populations. Immuno-STAT (Selective Targeting and Alteration of T cells) is a fusion protein platform comprising a bivalent peptide-major histocompatibility complex (MHC) class I complex and an affinity-attenuated IL-2 mutein that co-stimulates T-cell receptor and IL-2 signaling in epitope-specific CD8 T cells. Here, we investigated whether a D IMPORTANCE: Interleukin-2 (IL-2) is a key cytokine for promoting effector differentiation of antigen-specific CD8 T cells and remains an attractive agent in cancer immunotherapy, but systemic toxicity limits its clinical use. This study addresses a central challenge in IL-2-based immunotherapy: delivering IL-2 to cognate antigen-specific CD8 T cells while minimizing activation of non-targeted populations. Using a mouse model of chronic lymphocytic choriomeningitis virus (LCMV) infection, we show that the Immuno-STAT (Selective Targeting and Alteration of T cells) platform selectively expands targeted virus-specific CD8 T cells and enhances their function while limiting effects on non-targeted populations. We also show that combining Immuno-STAT with PD-1 blockade further enhances targeted virus-specific CD8 T-cell responses during chronic LCMV infection. These findings provide mechanistic and preclinical support for integrating T-cell receptor specificity with IL-2 signaling to advance cancer immunotherapy and guide next-generation IL-2 therapeutics for cancer and chronic infection.
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