El humo del cigarrillo altera las células T para promover el cáncer de páncreas

In this issue, Griffith and colleagues describe a novel mechanism by which exposure to the carcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin through cigarette smoking promotes pancreatic tumorigenesis via the orchestration of a tumor-permissive local T-cell compartment. By stimulating aryl hydrocarbon receptors in CD4+ T cells, 2,3,7,8-tetrachlorodibenzo-p-dioxin skews the pancreatic immune landscape toward tolerance by promoting the expansion of IL22-secreting Th22 cells and regulatory T cells while simultaneously depleting tumor-targeting CD8+ T cells, thereby accelerating pancreatic dysplasia and tumor progression. See related article by Griffith et al., p. 114.