急性髓系白血病患者中 TIGIT(+)CD226(-) γδ T 细胞升高

The diverse structural and functional heterogeneity of T cells is related to their distinct role in cancer immunity. The different phenotypes of T cells in patients with acute myeloid leukemia (AML) is far from clear. In particular, the expression pattern of co-inhibitory and co-stimulatory receptors on T cells remains unknown.

In this study, we analyzed the distribution of T cell subsets by expression of the immune checkpoint co-inhibitor TIGIT (T cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain) and its competing co-stimulatory receptor CD226 in AML patients of different clinical statuses (including de novo AML, AML in non-remission (NR), and AML in complete remission (CR)).

Our data demonstrated an imbalanced distribution of TIGIT and CD226 on T cells with a decrease in CD226 + T cells and an increase in TIGIT + T cells in de novo AML patients, while TIGIT - CD226 + T cells were restored in AML patients who achieved CR after chemotherapy.

Moreover, the patients who had higher TIGIT + CD226 - T cells showed lower overall survival rate for non-M3 AML, which may be considered a novel prognostic immune biomarker.

In conclusion, our study reveals for the first time that imbalance in the TIGIT/CD226 axis might be related to different clinical outcomes for AML patients.

Abbreviations : AML: acute myeloid leukemia; CR: complete remission; ICs: immune checkpoints; PD-1: programmed death-1; T cells: gamma delta T cells; TCR: T cell receptor; MHC: major histocompatibility complex; TIGIT: T cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain; NK: natural killer; PB: Peripheral blood; NR: non-remission; FAB: French-American-British; WHO: World Health Organization; HIs: healthy individuals; OS: overall survival.