Analysis reveals the interplay of autophagy-regulator BECN1 with T follicular cells in AML, suggesting prognostic relevance for remission.
Abstract Background Autophagy is a catabolic pathway with a controversial role regarding tumor suppression and promotion and is accused of suppressing the effect of several chemotherapeutic agents. Autophagy is also involved in regulating T cell function and immune response. This study aimed to characterize the interrelation of the autophagy-regulator gene BECN1 expression level with T follicular regulatory (Tfr) and T follicular helper (Tfh) cell ratio in acute myeloid leukemia (AML) and analyze their prognostic significance in achieving remission. Methods This study included 58 patients with denovo AML, and 26 controls. Levels of circulating Tfh and Tfr cells and analysis of fold change in BECN1 gene expression were evaluated in all participants. Patients were assessed whether they had achieved complete hematological remission after receiving induction chemotherapy or not. Results AML patients had significantly higher percentages of Tfh and Tfr cells and lower BECN1 gene expression level than the control group at the time of diagnosis. In addition, patients in the non-remission group showed a higher percentage of Tfr cells, Tfr/Tfh ratio, and BECN1 gene expression level than patients who achieved complete remission. Positive correlations were found between BECN1 expression level and both Tfr and Tfr/Tfh ratio. Conclusion the interplay between Tfh and Tfr cell imbalance and autophagy probably plays a pivotal role in AML pathogenesis and might be a good predictor of remission, eventually leading to improved outcomes and optimal treatment.
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Morsy et al. (2025) studied this question.
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