Correlation between acute myeloid leukemia and IL-17A, IL-17F, and IL-23R gene polymorphism.

Recent studies have shown that Th17 cells may be involved in the pathological process of acute myeloid leukemia. This CD4+ cell subgroup secretes highly homologous interleukin (IL)-17A and IL-17F, and also expresses IL-23 receptor (IL-23R) on the cell surface. Our study aims to investigate the relationship of IL-17A, IL-17F, and IL23R with disease susceptibility, and clarify the relationship between gene polymorphism variation and serum IL-17 level. 62 acute myeloid leukemia patients and 125 healthy controls were included in this study. Restriction fragment length polymorphism polymerase chain reaction (PCR-RFLP) was applied to analyze IL-17A (rs2275913; G-197A), IL17F (rs763780; A7488G; His161Arg), and IL-23R (rs11209026, G1142A; Arg381Gln) alleles. At the same time, enzyme-linked immunoassay analysis (ELISA) was used to test serum IL-17 level in patients. Acute myeloid leukemia patients presented higher rate of IL-17F G single mutant (RR=4.75, P<0.001) and GG mutation homozygote (RR=23.01, P<0.005). While IL-17A, IL-23R A single mutant and purified AA mutation homozygote showed no correlation with acute myeloid leukemia susceptibility. In addition, ELISA showed that serum IL-17 exhibited no significant difference between acute myeloid leukemia patients and healthy controls had (8.8±7.19 pg/ml vs. 1.4±0.2 pg/ml, P>0.05). IL-17F G single mutant and GG mutation homozygote were correlated with acute myeloid leukemia susceptibility, while IL-17 gene polymorphism and serum IL-17 level were not. Furthermore, IL-17A and IL-23R gene polymorphism were not associated with acute myeloid leukemia susceptibility.