Senescent T Cells: The Silent Culprit in Acute Myeloid Leukemia Progression?

Malignant tumors can evade immune surveillance and elimination through multiple mechanisms, with the induction of immune cell dysfunction serving as a crucial strategy. Mounting evidence indicates that T cell senescence constitutes the primary mechanism underlying T cell dysfunction in acute myeloid leukemia (AML) and represents one of the potential causes of immunotherapy failure. AML usually progresses rapidly and is highly susceptible to drug resistance, thereby resulting in recurrence and patient mortality. Hence, disrupting the immune interface within the bone marrow microenvironment of AML has emerged as a critical objective for synergistically enhancing tumor immunotherapy. In this review, we summarize the general characteristics, distinctive phenotypes, and regulatory signaling networks of senescent T cells and highlight their potential clinical significance in the bone marrow microenvironment of AML. Additionally, we discuss potential therapeutic strategies for alleviating and reversing T cell senescence.