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FT538,即诱导多能干细胞衍生的自然杀伤细胞,与化疗联合使用时可增强对急性髓系白血病细胞的杀伤作用。

FT538, iPSC-derived NK cells, enhance AML cell killing when combined with chemotherapy.

作者信息

Eckstrom Amanda, Tyagi Anudishi, Mahmood Sajid, Wong Lilly, Valamehr Bahram, Rao Adishwar, Agrawal Akriti, Siddiqui Maryam, Battula V Lokesh

机构信息

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Fate Therapeutics, Inc., San Diego, California, USA.

出版信息

J Cell Mol Med. 2025 Jan;29(1):e70169. doi: 10.1111/jcmm.70169.

Abstract

Induced pluripotent stem cell (iPSC)-derived natural killer (NK) cells offer an opportunity for a standardized, off-the-shelf treatment with the potential to treat a wider population of acute myeloid leukaemia (AML) patients than the current standard of care. FT538 iPSC-NKs express a high-affinity, noncleavable CD16 to maximize antibody dependent cellular cytotoxicity, a CD38 knockout to improve metabolic fitness, and an IL-15/IL-15 receptor fusion preventing the need for cytokine administration, the main source of adverse effects in NK cell-based therapies. Here, we sought to evaluate the potential of FT538 iPSC-NKs as a therapy for AML through their effect on AML cell lines and primary AML cells. We observed that FT538 iPSC-NKs induce effector-to-target cell ratio dependent apoptosis in cell lines and primary AML cells, including cells from high-risk patients. Flow cytometric analysis revealed that FT538 iPSC-NKs induce AML cell death when combined with the AML therapies: cytarabine, venetoclax and gilteritinib. Moreover, cytarabine did not affect FT538 iPSC-NK viability, suggesting that iPSC-derived NK therapies and chemotherapy may be a promising treatment combination. This study provides the basis for further study of iPSC-derived NK cell therapies as a treatment option for high-risk AML patients, particularly those with disease resistant to standard therapies.

摘要

诱导多能干细胞(iPSC)衍生的自然杀伤(NK)细胞为标准化的现成治疗提供了机会,有可能治疗比当前标准治疗更广泛的急性髓系白血病(AML)患者群体。FT538 iPSC-NK细胞表达一种高亲和力、不可裂解的CD16,以最大化抗体依赖性细胞毒性,敲除CD38以改善代谢适应性,并表达一种白细胞介素15/白细胞介素15受体融合蛋白,从而无需给予细胞因子,而细胞因子是基于NK细胞疗法中不良反应的主要来源。在此,我们试图通过FT538 iPSC-NK细胞对AML细胞系和原发性AML细胞的作用来评估其作为AML治疗方法的潜力。我们观察到,FT538 iPSC-NK细胞在细胞系和原发性AML细胞(包括高危患者的细胞)中诱导效应细胞与靶细胞比例依赖性凋亡。流式细胞术分析显示,当与AML治疗药物阿糖胞苷、维奈克拉和吉瑞替尼联合使用时,FT538 iPSC-NK细胞可诱导AML细胞死亡。此外,阿糖胞苷不影响FT538 iPSC-NK细胞的活力,这表明iPSC衍生的NK细胞疗法与化疗可能是一种有前景的治疗组合。本研究为进一步研究iPSC衍生的NK细胞疗法作为高危AML患者(尤其是对标准疗法耐药的患者)的治疗选择提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28cf/11724334/8203fb1d82cc/JCMM-29-e70169-g003.jpg

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