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10.18632/oncotarget.11179

http://scihub22266oqcxt.onion/10.18632/oncotarget.11179
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C5308636!5308636!27517629
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suck abstract from ncbi


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pmid27517629      Oncotarget 2016 ; 7 (38): 61069-80
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  • Exogenous IL-33 overcomes T cell tolerance in murine acute myeloid leukemia #MMPMID27517629
  • Qin L; Dominguez D; Chen S; Fan J; Long A; Zhang M; Fang D; Zhang Y; Kuzel TM; Zhang B
  • Oncotarget 2016[Sep]; 7 (38): 61069-80 PMID27517629show ga
  • Emerging studies suggest that dominant peripheral tolerance is a major mechanism of immune escape in disseminated leukemia. Using an established murine acute myeloid leukemia (AML) model, we here show that systemic administration of recombinant IL-33 dramatically inhibits the leukemia growth and prolongs the survival of leukemia-bearing mice in a CD8+ T cell dependent manner. Exogenous IL-33 treatment enhanced anti-leukemia activity by increasing the expansion and IFN-? production of leukemia-reactive CD8+ T cells. Moreover, IL-33 promoted dendritic cell (DC) maturation and activation in favor of its cross presentation ability to evoke a vigorous anti-leukemia immune response. Finally, we found that the combination of PD-1 blockade with IL-33 further prolonged the survival, with half of the mice achieving complete regression. Our data establish a role of exogenous IL-33 in reversing T cell tolerance, and suggest its potential clinical implication into leukemia immunotherapy.
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