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- W94172949 abstract "Abstract An important challenge in the therapy of immune-mediated inflammatory diseases is to control established disease, largely because autoreactive memory T lymphocytes are difficult to suppress or eliminate. Memory T cells depend on interleukin-7 (IL-7) for their generation and maintenance and genomic studies have associated the cytokine’s receptor, IL-7Rα, with increased risk for autoimmune diseases such as type 1 diabetes. Here we show that IL-7Rα blockade reverses hyperglycemia in the non-obese diabetic (NOD) mouse model of type 1 diabetes. Diabetogenic memory T cells deprived of IL-7 signals remained present in the lymphoid organs but expressed the inhibitory molecule Programmed Death 1 (PD-1), which is critical for preventing autoimmunity. Blocking the interaction of PD-1 with its ligand, PD-L1, in cured mice rapidly induced hyperglycemia, demonstrating that this mechanism inhibited memory responses to pancreatic islets after IL-7Rα blockade. Conversely, IL-7 suppressed PD-1 expression after T cell activation, indicating that IL-7 contributes to the pathogenesis of autoimmune diabetes by keeping memory T cells in a functionally competent, tolerance-resistant state. Our data uncover a novel link between IL-7 and the PD-1/PD-L1 tolerance pathway and identify IL-7Rα blockade as a potential therapeutic approach to induce PD-1-mediated inhibition of pathogenic memory T cells in established T cell-dependent inflammatory diseases." @default.
- W94172949 created "2016-06-24" @default.
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- W94172949 date "2011-04-01" @default.
- W94172949 modified "2023-09-23" @default.
- W94172949 title "Interleukin-7 promotes autoimmune disease by enabling memory T cells to escape PD-1-mediated tolerance (164.21)" @default.
- W94172949 doi "https://doi.org/10.4049/jimmunol.186.supp.164.21" @default.
- W94172949 hasPublicationYear "2011" @default.
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