ArticleThe clinical respiratory journal2025
IL-15 Superagonist SHR-1501 Enhances Immune Responses in Lung Cancer by Modulating Tumor Microenvironment.
Article in The clinical respiratory journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- PEG-RLI: A Long-Acting IL-15 Agonist That Produces Massive Levels of CD8Pharmaceutics · 2026Article
- Targeting inflammatory microenvironments: overcoming therapy resistance and immunosuppression.Molecular cancer · 2026Review
- Immune interception in cancer: prioritizing vaccination in high-risk and premalignant settings.Frontiers in immunology · 2026Article
- IL-15 Superagonist SHR-1501 Enhances Immune Responses in Lung Cancer by Modulating Tumor Microenvironment.The clinical respiratory journal · 2025Article
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6 authors.
Funding
Abstract
backgroundInterleukin-15 (IL-15) is a pleiotropic cytokine recognized as a promising therapeutic agent in cancer immunotherapy. IL-15 superagonists have shown efficacy across various cancers, yet their effects in lung cancer immunotherapy remain underexplored.
methodsThis study evaluated the antitumor effects of SHR-1501 through intratumoral injection in two murine lung cancer models: Lewis lung carcinoma (LLC) and Kras G12D/p53-/- (KP). We employed flow cytometry to assess immune cell populations in the tumor microenvironment (TME) and systemic circulation. Immunohistochemistry (IHC) was used to analyze TME changes in tumor tissues, while single-cell RNA sequencing provided insights into TME modulation following SHR-1501 treatment. Additionally, we assessed the synergistic potential of combining SHR-1501 with PD-1 monoclonal antibody (mAb) therapy and explored the abscopal effect of SHR-1501.
resultsSHR-1501 significantly inhibited tumor growth in both KP and LLC models at 5 μg and 15 μg doses (p = 0.0022 and p = 0.0002, respectively, for KP; p = 0.0508 and p = 0.0131, respectively, for LLC). Flow cytometry revealed increased infiltration of CD8+ T cells, effector memory CD8+ T cells (TEM), and natural killer (NK) cells in the TME. SHR-1501 also enhanced systemic immune responses, increasing CD8+ T cells and TEM populations in peripheral blood and spleen, with an early NK cell elevation on day 7 post-treatment. Single-cell analysis indicated that SHR-1501 promoted the activity of macrophages, increasing M1 macrophage proportions. Moreover, SHR-1501 enhanced the antitumor immune response by promoting pro-inflammatory changes across multiple cell types within the TME, including neutrophils, fibroblasts, and endothelial cells. When combined with PD-1mAb, SHR-1501 exhibited potent synergistic antitumor effects. The combination therapy significantly prolonged overall survival with no significant toxicity observed. Furthermore, SHR-1501 may have the ability to induce an abscopal effect.
conclusionSHR-1501 demonstrated potent antitumor activity, especially when combined with PD-1 mAb. Its mechanism likely involves promoting CD8+ T cell and NK cell infiltration and enhancing M1 macrophage activity. These findings provide evidence for further clinical trials exploring SHR-1501 in nonsmall cell lung cancer (NSCLC) therapy.
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