Correlation of the transcription factors <i>IRF4</i> and <i>BACH2</i> with the abnormal <i>NFATC1</i> expression in T cells from chronic myeloid leukemia patients

T cell dysfunction is a common characteristic of patients with myeloid leukemia and is closely related to clinical efficacy and prognosis. In order to clarify the mechanisms leading to the T cell dysfunction, we characterized the gene expression profile of T cells from chronic myelogenous leukemia (CML) patients by microarray analysis and investigated the related regulating pathway. We employed gene expression profiling, bioinformatics and real-time quantitative reverse transcription PCR (RT-qPCR) to detect genes differentially expressed in CML patients versus healthy donors. There were 1704 genes differentially expressed between CD3⁺ T cells from CML patients and healthy donors, including 868 up-regulated genes and 836 down-regulated genes, which mostly related to T cell functional pathways. In particular, lower expression of <i>NFATC1</i>, a member of the TCR signaling pathway, was detected in CD3⁺ T cells from CML patients. We further found that the expression of <i>IRF4</i> and <i>BACH2</i>, transcription factors that potentially regulate <i>NFATC1</i>, in CD3⁺ T cells from CML patients was significantly lower than that in healthy donors. We for the first time observed the altered gene expression profiles of CD3⁺ T cells from CML patients, and the results suggested that <i>IRF4</i>, <i>BACH2</i> and <i>NFATC1</i> may be involved in regulating T cell dysfunction in CML patients in the form of a transcriptional regulatory network. These findings may provide potential targets for tyrosine kinase inhibitors in combination with other targeted immunotherapies .