In this issue of Blood, Herrmann et al1 have developed a novel checkpoint inhibitory T-cell–engaging (CiTE) antibody for acute myeloid leukemia (AML) by fusing the extracellular domain of programmed cell death protein 1 (PD-1ex) to a CD3 3 CD33 bispecific T-cell engager (BiTE; see figure panels A-B). Incorporation of the PD-1ex domain increased human T-cell activation and led to efficient cytotoxicity against CD331/PD-L11 cells in vitro and in a murine xenograft model. Importantly, the PD-1ex domain is not sufficient to redirect T cells to PD-L11 cells lacking the CD33 target. This preferential targeting of CD331/PD-L11 cells should reduce the immune-related adverse events associated with on-target/off-tumor effects of global checkpoint blockade with anti-PD1/PD-L1 monoclonal antibodies (mAbs).

Original languageEnglish
Pages (from-to)2425-2427
Number of pages3
Issue number23
StatePublished - Dec 6 2018


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