Regulatory T cells‐derived IL‐35 promotes the growth of adult acute myeloid leukemia blasts. Issue 10 (6th August 2015)

• Record Type: Journal Article
• Authors: Tao, Qianshan; Pan, Ying; Wang, Yiping; Wang, Huiping; Xiong, Shudao; Li, Qing; Wang, Jia; Tao, Lili; Wang, Zhitao; Wu, Fan; Zhang, Rui; Zhai, Zhimin
• Is Part Of: International journal of cancer. Volume 137:Issue 10(2015:Nov. 15)
• Page Start: 2384
• Page End: 2393
• Publication Date: 2015-08-06
• Subjects: Cancer -- Periodicals; Cancer -- Prevention -- Periodicals; 616.994
• DOI: 10.1002/ijc.29563
• Languages: English
• ISSNs: 0020-7136

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>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.</p> </abstract>