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This study aimed to characterize the presence, phenotype, and functional role of MAIT cells in PDAC and explore the underlying regulatory mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We analyzed human PDAC tissue samples using single-cell RNA sequencing and flow cytometry to evaluate MAIT cell abundance and phenotype. Functional studies were performed in MR1-deficient (\n                      <jats:italic>Mr1<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>\u2212\/\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      ) mice to assess the impact of MAIT cell deficiency on tumor-associated macrophage polarization. Cytokine profiling and signaling analyses were used to investigate mechanisms of MAIT cell activation within the tumor microenvironment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      MAIT cells were significantly enriched in PDAC tissues and associated with poor patient survival. Further studies inMR1-deficient (\n                      <jats:italic>Mr1<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>\u2212\/\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      ) mice demonstrated that the absence of MAIT cells markedly attenuated M2 macrophage polarization. Mechanistically, tissue-resident MAIT cells secreted higher levels of CSF-1 versus circulating subsets. This phenomenon suggests that MAIT cells may be reprogrammed by the tumor microenvironment. Building on this, we discovered that Ttumor-derived TL1A activated MAPK signaling in MAIT cells, potentiating CSF-1 secretion.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings reveal a novel TL1A-MAIT-CSF-1 axis that drives immunosuppression in PDAC by reprogramming innate immune responses. Targeting MAIT cells or TL1A signaling may represent a promising therapeutic strategy to improve immunotherapy efficacy in PDAC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00535-026-02468-4","type":"journal-article","created":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T09:32:28Z","timestamp":1782293548000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Mucosal-associated invariant T cells promote PDAC progression via TL1A\u2013CSF-1 axis"],"prefix":"10.1007","author":[{"given":"Longyun","family":"Ye","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qinglin","family":"Fei","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tianjiao","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huiyi","family":"Ou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuai","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yiting","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xianjun","family":"Yu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaizhou","family":"Jin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7188-1066","authenticated-orcid":false,"given":"Weiding","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,6,24]]},"reference":[{"issue":"1","key":"2468_CR1","doi-asserted-by":"publisher","first-page":"10","DOI":"10.3322\/caac.21871","volume":"75","author":"RL Siegel","year":"2025","unstructured":"Siegel RL, Kratzer TB, Giaquinto AN, Sung H, Jemal A. 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