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Blood:双功能的PD-1xαCD33xαCD33融合蛋白可逆转急性髓系白血病的适应性免疫逃逸

2018-10-07 MedSci MedSci原创

靶向CD33的双特异性T细胞衔接器(BiTER)AMG330,在体外和小鼠模型中均被证明可高效调节急性髓系白血病(AML)细胞的细胞溶解。但T细胞激活与PD-L1和AML细胞上的其他抑制检查点上调相关,而PD-L1和抑制检查点上调又会导致适应性免疫耐受。PD1和PD-L1阻滞剂或许可中和T细胞功能障碍,但是,这会导致广泛的免疫相关的副反应(irAEs)。Monika Herrmann等人开发出一种

靶向CD33的双特异性T细胞衔接器(BiTER)AMG330,在体外和小鼠模型中均被证明可高效调节急性髓系白血病(AML)细胞的细胞溶解。但T细胞激活与PD-L1和AML细胞上的其他抑制检查点上调相关,而PD-L1和抑制检查点上调又会导致适应性免疫耐受。PD1和PD-L1阻滞剂或许可中和T细胞功能障碍,但是,这会导致广泛的免疫相关的副反应(irAEs)。

Monika Herrmann等人开发出一种双重功能的检查点抑制T细胞结合(CiTE)抗体,该抗体可促进T细胞与AML上的CD33结合,同时局部限制免疫检查点封闭。这一点是通过融合PD-1的胞外结构域(PD-1ex)实现的,PD-1ex对PD-L1、αCD3.αCD33BiTER样支架的自然亲和力较低。通过检查点封闭和亲和力依赖性锚定的协同效应,PD-1ex连接体增强了T细胞激活(IFN-γ升高3.3倍),同时促进针对CD33+PD-L1+细胞系和患者来源的AML细胞产生高选择性高效的细胞毒性作用。在小鼠移植瘤模型中,CiTE可诱导完全消除AML,且无免疫相关副反应的初始迹象,即体重减轻。

综上所述,Monika Herrmann等人开发出的分子可优先靶向AML细胞,而高亲和力阻滞剂,如临床所批准的抗癌药,同时会靶向PD-L1+的非AML细胞。通过在一个单分子中结合免疫检查点封闭和T细胞激活的高效性,研究人员有望将与系统应用免疫检查点抑制剂相关的irAEs降至最低,为患者提供高潜能的治疗方案,特别是复发型/难治性AML患者。


原始出处:

Monika Herrmann,et al.Bifunctional PD-1 x αCD3 x αCD33 fusion protein reverses adaptive immune escape in acute myeloid leukemia. Blood  2018  :blood-2018-05-849802;  doi: https://doi.org/10.1182/blood-2018-05-849802

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    2018-10-10 衣带渐宽

    学习

    0

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    2018-10-09 licz0427
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    2018-10-09 智智灵药
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