髓系白血病
发病机制
细胞因子
癌症研究
白血病
免疫学
白细胞介素2受体
免疫系统
髓样
效应器
生物
医学
T细胞
作者
Qianshan Tao,Ying Pan,Yiping Wang,Huiping Wang,Shudao Xiong,Qing Li,Jia Wang,Lili Tao,Zhitao Wang,Fan Wu,Rui Zhang,Zhimin Zhai
摘要
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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