MD Anderson team finds CD64 pathway lets T cells kill AML without MHC

Researchers at The University of Texas MD Anderson Cancer Center report that T cells can destroy acute myeloid leukemia cells through a CD64-dependent route that still needs an intact T cell receptor but does not require conventional MHC recognition, SciTechDaily reported. The PNAS study, led by Cassian Yee and Kapil Saxena, found activated T cells still killed AML cells after MHC was removed across cell lines and primary patient samples, including relapsed and high-risk mutation cases. Removing TCRs from the T cells stopped the killing, and NK-related pathways did not explain the effect. A genome-wide CRISPR screen pointed to CD64 and interferon-gamma signaling genes. Removing CD64 made AML cells resistant; adding CD64 to resistant cells increased vulnerability. The authors link the route to possible reasons AML can respond to stem cell transplantation and plan further work on CD64-TCR interaction for T cell therapies. Reference line cited by SciTechDaily: Kapil Saxena et al., 13 July 2026, Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.2601232123.