A fully human pan VL9 HLA-E TCRm antibody enables functional dissection of HLA-E biology and checkpoint signaling

. Using ABX002, we reveal that canonical VL9/HLA-E surface expression is tightly controlled by inflammatory cues, remarkably infrequent on tumors without stimulation, and almost absent from immune cells except myeloid-lineage cells. ABX002 unlocks cell-type and context-specific quantification of HLA-E antigen presentation, providing unprecedented insight into immune evasion and regulation. It additionally disrupts the NKG2A checkpoint, restoring cytotoxic lymphocyte function and enabling mechanistic and therapeutic mapping of HLA-E restricted peptide presentation. Together, these findings position ABX002 as a transformative tool for dissecting the landscape and biology of canonical peptide restriction in cancer immunity.