Downregulation of MICA/MICB improves cell persistence and clinical activity of NKG2DL CAR T-cells in patients with relapsed or refractory acute myeloid leukemia or myelodysplastic neoplasia



Summary

CAR T-cell therapy targeting NKG2D ligands (NKG2DLs) MICA/MICB shows promise in treating relapsed/refractory acute myeloid leukemia (AML) and myelodysplastic neoplasia (MDS). However, some AML/MDS cells shed MICA/MICB, potentially leading to CAR T-cell exhaustion and reduced effectiveness. This study demonstrates that downregulation of MICA/MICB in AML/MDS cells enhances CAR T-cell persistence and clinical activity. By selecting for AML/MDS cells with lower MICA/MICB expression, researchers observed improved CAR T-cell engraftment, prolonged survival, and enhanced clinical responses in patients. This suggests that targeting AML/MDS cells with downregulated MICA/MICB could be a strategy to improve the efficacy of NKG2DL CAR T-cell therapy.

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