Abstract
Acute myeloid leukemia (AML) establishes an immunosuppressive microenvironment that favors leukemic proliferation. The immune-suppressive cytokines altered antigen processing, and presentation collectively assist AML cells in escaping cytotoxic T-cell surveillance. These CD8(+) T cell dysfunction features are emerging therapeutic targets in relapsed/refractory AML patients. Besides, CD8(+) T cell exhaustion is a hotspot in recent clinical oncology studies, but its pathophysiology has yet to be elucidated in AML. In this review, we summarize high-quality original studies encompassing the phenotypic and genomic characteristics of T cell exhaustion events in the leukemia progression, emphasize the surface immuno-peptidome that dynamically tunes the fate of T cells to function or dysfunction states, and revisit the biochemical and biophysical properties of type 1 MHC antigen processing mechanism (APM) that pivots in the phenomenon of leukemia antigen dampening.