ArticleProceedings of the National Academy of Sciences of the United States of America2024
Intratumoral NKT cell accumulation promotes antitumor immunity in pancreatic cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Gut Microbiota-Immune Interactions in Endometrial Cancer: Causal Mediation and Subtype-Specific Mechanisms.International journal of women's health · 2026Article
- Quantitative analysis of lymphocyte exhaustion markers in patients with localized clear cell renal cell carcinoma.Oncology letters · 2025Article
- Facilitation of natural killer T-cell cytotoxic activity in uterine sarcoma via theTranslational cancer research · 2025Article
- NKT cells-a generalist in disease treatment and a new key to unlock immunotherapy.Immunotherapy · 2025Review
- Multi-omics analysis reveals ultraviolet response insights for immunotherapy and prognosis.Frontiers in immunology · 2025Article
- An integrated analysis identified mitochondrial ribosomal protein MRPL3 as a potential prognostic biomarker and therapeutic target in pancreatic cancer.Journal of Cancer · 2025Article
- Intratumoral NKT cell accumulation promotes antitumor immunity in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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Authors and funding
3 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDA) is a potentially lethal disease lacking effective treatments. Its immunosuppressive tumor microenvironment (TME) allows it to evade host immunosurveillance and limits response to immunotherapy. Here, using the mouse KRT19-deficient (sgKRT19-edited) PDA model, we find that intratumoral accumulation of natural killer T (NKT) cells is required to establish an immunologically active TME. Mechanistically, intratumoral NKT cells facilitate type I interferon (IFN) production to initiate an antitumor adaptive immune response, and orchestrate the intratumoral infiltration of T cells, dendritic cells, natural killer cells, and myeloid-derived suppressor cells. At the molecular level, NKT cells promote the production of type I IFN through the interaction of their CD40L with CD40 on myeloid cells. To evaluate the therapeutic potential of these observations, we find that administration of folinic acid to mice bearing PDA increases NKT cells in the TME and improves their response to anti-PD-1 antibody treatment. In conclusion, NKT cells have an essential role in the immune response to mouse PDA and are potential targets for immunotherapy.
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