Authors
Makiko Suga, Shuhei Kida, Yo Mizutani, Yosuke Kogue, Yuta Yamaguchi, Shunya Ikeda, Ryuhei Kawamoto, Mana Tachikawa, Tsubasa Seto, Hiroto Takekawa, Yuto Maehara, Kumi Shibata, Kazuhito Tsutsumi, Hiraku Murakami, Emiko Mizuta, Kyoko Yoshihara, Satoshi Yoshihara, Hirohisa Nakamae, Takafumi Nakao, Megumu Inoue, Shuji Ueda, Satoru Kosugi, Yasutaka Ueda, Hisashi Kato, Shinsuke Kusakabe, Hidenori Kasahara, Akihisa Hino, Jiro Fujita, Tomoaki Ueda, Michiko Ichii, Kentaro Fukushima, Naoki Hosen
Published in
Haematologica. Oct 15, 2026. Epub Oct 15, 2026.
Abstract
CAR NK cell therapy is expected to be developed to treat acute myeloid leukemia (AML). C-type lectin-like molecule 1 (CLL-1) is a candidate target. However, AML cells with minimal CLL-1 expression (CLL-1dim) may not be eliminated by CAR NK cells. Here we demonstrate that cord blood (CB)-derived NK cells transduced with a novel high-affinity CAR that recognizes CLL-1 can eliminate CLL-1dim AML cells. A newly established anti- CLL-1 monoclonal antibody (mAb) designated as 2-23 exhibits a higher affinity for CLL- 1 than the widely used anti-CLL-1 mAb M26. CB-derived NK cells transduced with a CAR derived from 2-23, but not M26, killed CLL-1dim AML cells in vitro. Additionally, treatment with 2-23 CAR NK cells, but not M26 CAR NK cells, significantly enhanced the survival of the mice transplanted with CLL-1dim AML cells in vivo. Furthermore, in AML patient-derived xenograft models, the 2-23 CAR NK cells expanded robustly, persisted, and eradicated AML cells.
PMID:
42876290
Bibliographic data and abstract were imported from PubMed on 15 Oct 2026.
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