Journal
INTERNATIONAL JOURNAL OF CANCER
Volume 137, Issue 10, Pages 2384-2393Publisher
WILEY-BLACKWELL
DOI: 10.1002/ijc.29563
Keywords
acute myeloid leukemia; immune escape; regulatory T cells; IL-35
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Funding
- National Natural Science Foundation of China [81401293]
- Higher School of Anhui Provincial Natural Science Research Project [KJ2013Z121, KJ2014Z017]
- Natural Science Foundation of Anhui Medical University [2015XKJ018]
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Tumor immune escape mechanism mediated by CD4+CD25+regulatory T cells (Tregs) is a key factor in the pathogenesis of acute myeloid leukemia (AML). IL-35, as a novel inhibitory cytokine, is produced by Tregs specially and regulates functions of Tregs in murine. However, IL-35 expression of Tregs in human is still disputed, and its role in AML is yet to be elucidated. In this study, we found that IL-35 was expressed highly in peripheral blood plasma of adult patients with AML and significantly correlated with the clinical stages of malignancy. Tregs-derived from adult AML patients produced IL-35 in a stimulation-dependent manner. IL-35 promoted AML blasts immune escape by expanding Tregs and inhibiting CD4+CD25-effector T cells (Teffs). Furthermore, IL-35 directly promoted the proliferation of AML blasts and reduced the apoptosis of AML blasts. Together, our study demonstrates that IL-35-derived from Tregs promotes the growth of adult AML blasts, suggesting that IL-35 has an important role in the pathogenesis of AML.
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