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High expression of Galectin‐1 in pancreatic stellate cells plays a role in the development and maintenance of an immunosuppressive microenvironment in pancreatic cancer

Galectin‐1 is implicated in making tumor cells immune privileged, in part by regulating the survival of infiltrating T cells. Galectin‐1 is strongly expressed in activated pancreatic stellate cells (PSCs); however, whether this is linked to tumor cell immune escape in pancreatic cancer is unknown. Galectin‐1 was knocked down in PSCs isolated from pancreatic tissues using small interfering RNA (siRNA), or overexpressed using recombinant lentiviruses, and the PSCs were cocultured with T cells. CD3+, CD4+ and CD8+ T cell apoptosis was detected by flow cytometry; T cell IL‐2, IL‐4, IL‐5 and INF‐γ production levels were quantified using ELISA. Immunohistochemical analysis showed increased numbers of PSCs expressed Galectin‐1 (p < 0.01) and pancreatic cancers had increased CD3+ T cell densities (p < 0.01) compared to normal pancreas or chronic pancreatitis samples. In coculture experiments, PSCs that overexpressed Galectin‐1 induced apoptosis of CD4+ T cells (p < 0.01) and CD8+ T cells (p < 0.05) significantly, compared to normal PSCs. Knockdown of Galectin‐1 in PSCs increased CD4+ T cell (p < 0.01) and CD8+ T cell viability (p < 0.05). Supernatants from T cells cocultured with PSCs that overexpressed Galectin‐1 contained significantly increased levels of Th2 cytokines (IL‐4 and IL‐5, p < 0.01) and decreased Th1 cytokines (IL‐2 and INF‐γ, p < 0.01). However, the knockdown of PSC Galectin‐1 had the opposite effect on Th1 and Th2 cytokine secretion. Our study suggests that the overexpression of Galectin‐1 in PSCs induced T cell apoptosis and Th2 cytokine secretion, which may regulate PSC‐dependent immunoprivilege in the pancreatic cancer microenvironment. Galectin‐1 may provide a novel candidate target for pancreatic cancer immunotherapy.