Abstract
Acute myeloid leukemia (AML) is a hematological tumor in which progress T helper (Th) subsets including Th22, Th17, and Th1 cells play a pivotal role. However, the role of T helper (Th) subsets in the immune pathogenesis of AML remains unclear. Here, we investigated frequencies of Th22, Th17, pure Th17, and Th1 cells in the peripheral blood (PB) of AML patients. We demonstrated that Th22, Th17, and pure Th17 in newly-diagnosed (ND) and non-complete remission (Non-CR) AML patients and plasma IL-22 in ND AML patients were significantly increased. Retinoid-related orphan receptor C (RORC) expression was significantly elevated in CR and Non-CR AML patients. However, Th1 in ND AML patients and IL-17 in ND, Non-CR or CR AML patients was significantly decreased compared with controls. Moreover, Th22 and IL-22 showed positive correlation with pure Th17, but Th22 showed negative correlation with Th1 in ND AML patients. RORC showed positive correlation with Th22 and approximately positive correlation with pure Th17 in Non-CR patients. PB blast cell showed positive correlation with Th22 and negative correlation with Th1 in ND AML patients. Our results indicate that Th22 and pure Th17 cells conjointly contribute to the pathogenesis of AML and might be promising novel clinical index for AML.
Highlights
Acute myeloid leukemia (AML) is a disease with malignant clone of hematopoietic stem cells, characterized by the accumulation of considerable immature myeloblasts in bone marrow
It is well known that persistent immunodeficiency is a common feature in patients with leukemia and T cell function becomes suppressed as the disease progresses [33,34]
IL-22 showed a positive correlation with pure Th17 cells in ND AML patients
Summary
Acute myeloid leukemia (AML) is a disease with malignant clone of hematopoietic stem cells, characterized by the accumulation of considerable immature myeloblasts in bone marrow. It has been shown that Th22 cells play an important and complicated role in some inflammatory and autoimmune diseases [18,24]. Recent studies show that IL-22 has been implicated in the etiology of inflammatory and autoimmune diseases [25,28,29,30], myelodysplastic syndrome (MDS) [31] and T-cell. (CD4+IFN-γ−IL-22−IL17+), and Th1 cells (CD4+IFN-γ+), plasma IL-22 or IL-17 levels and mRNA expression of RORC in peripheral blood (PB) of AML patients. Their correlations with disease activity were evaluated in the present study
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