In this issue of Blood, Gillissen and colleagues characterize donor-derived cytotoxic antibodies, isolated from allogeneic hematopoietic cell transplant (HSCT) patients with acute myelogenous leukemia (AML) in sustained remission, that targeted the spliceosome U5 snRNP200 complex expressed on the cell membrane of AML blasts. Mechanistically, in vitro antibody-dependent cytotoxicity did not cause leukemia cell apoptosis, but rather destabilization of the cell membrane cytoskeleton and subsequent pore formation, resulting in cellular swelling and extravasation of intracellular contents (oncosis). In addition, in vivo reduction in AML burden using a U5 snRNP200–specific antibody was demonstrated in a murine SCID xenograft model. Collectively, the authors’ work suggests a potential role for donor-derived antibodies in mediating graft-versus-leukemia (GVL) activity following allogeneic HSCT.1

中文翻译：

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反洗钱：暴露和利用？

在本期血液杂志中，Gillissen 及其同事描述了从持续缓解的急性髓性白血病 (AML) 的同种异体造血细胞移植 (HSCT) 患者中分离的供体来源的细胞毒性抗体，该抗体靶向表达在细胞膜上的剪接体 U5 snRNP200 复合物。 AML 爆炸。从机制上讲，体外抗体依赖性细胞毒性不会导致白血病细胞凋亡，而是导致细胞膜细胞骨架不稳定和随后的孔形成，导致细胞肿胀和细胞内内容物外渗（肿胀）。此外，在小鼠 SCID 异种移植模型中证明了使用 U5 snRNP200 特异性抗体在体内减少 AML 负担。总的来说，