Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
Acute myeloid leukemia (AML) is the most common hematological malignancy in adults, characterized by distorted proliferation and development of myeloid cells and their precursors in blood and bone marrow. Impressive biologic advances have increased our understanding of leukemogenesis, however, little is known about the pathogenic events which lead to the initiation and progression of AML. T helper type 17 (Th17) cells are a unique subset of CD4+ T cells. They play important roles in the pathogenesis of many diseases, including inflammatory diseases, autoimmune diseases, and cancers. A range of cytokines, such as interleukin (IL)-23, transforming growth factor-beta (TGF-beta), IL-1beta, IL-6, IL-17, IL-22, and IL-21, have been shown related to Th17 cells. Some researchers have reported that the levels of Th17 and its related cytokines were different between normal cells and malignant AML cells, suggesting that Th17 might be involved in AML pathogenesis. In this review, we summarize current progress in the mechanisms of Th17 related cytokines in AML pathogenesis.