Nature medcine:CD47是癌症免疫检查点疗法的新型靶点

2015-10-13 佚名 生物谷

CD47主要表达于癌细胞表面,通常被认为是癌细胞免于宿主免疫系统攻击的保护性受体。最近一项研究表明T细胞与树突状细胞(DC)可以通过CD47阻断效应发挥抗肿瘤的效应。   巨噬细胞发挥吞噬效应需要两个信号同时起作用:一个是靶向细胞表面的"eat me"信号的激活,另一个是同意目标表面"don't eat me"信号的失活。任何一个信号的缺少都不足以引发吞噬效应的发生。越来越多的证

CD47主要表达于癌细胞表面,通常被认为是癌细胞免于宿主免疫系统攻击的保护性受体。最近一项研究表明T细胞与树突状细胞(DC)可以通过CD47阻断效应发挥抗肿瘤的效应。
 
巨噬细胞发挥吞噬效应需要两个信号同时起作用:一个是靶向细胞表面的"eat me"信号的激活,另一个是同意目标表面"don't eat me"信号的失活。任何一个信号的缺少都不足以引发吞噬效应的发生。越来越多的证据表明,CD47是一类"don't eat me"信号,它通过与巨噬细胞表面的SIRP-α相互结合抑制巨噬细胞的同能。CD47作为癌症治疗的靶点具有不可比拟的优势:1.它广泛地表达于各类癌细胞表面,因此可以用于治疗各种类型的癌症;2. 正常细胞由于缺乏"eat me"signal,因此单单阻断CD47并不能引发巨噬细胞对正常细胞的吞噬效应,因此CD47阻断剂的副作用也十分小。前期的基础实验数据已经支持了这一观点。他们通过小鼠异体肿瘤移植模型说明了CD47阻断的有效性与安全性。事实上,目前已经有许多CD47抗体类药物进入了临床试验阶段。
 
然而,最近在nature medcine杂志上。来自芝加哥大学的Meng Michelle Xu研究组报道了CD47阻断疗法中,CD8+T细胞与DC的抗癌效应。他们提供证据证明在CD47被阻断后,DC的激活与T细胞的priming也随随之激活。利用自体小鼠癌症模型,Xu等人证明了CD47阻断的抗癌效应最终是由CD8+T细胞完成的。他们发现在患有肿瘤的T细胞缺失小鼠中,CD47的抗癌效应消失不见了。由于CD8+T细胞的激活依赖于抗原呈递细胞表面MHC-I的传递,因此作者又研究了是否巨噬细胞或树突状细胞参与了这一过程。通过体内与体外实验,作者们发现这一抗原呈递效应主要由树突状细胞参与,而且主要依赖于DC内部的DNA感受分子元件-STING,而非传统的模式识别受体TOLL,以及MyD88。然而,是否CD4+T细胞以及MHC-II是否参与了CD47阻断介导的抗癌过程仍然是未知的问题。
 
至于在应用方面,CD47阻断剂的关键问题在于其安全性。由于CD47广泛表达于肿瘤组织与正常组织表面,因此需要谨慎的设计保证其在杀伤肿瘤的同时不威胁正常细胞的安全。另外还需要考虑的问题是它的安全有效性,比如CD47阻断剂能否顺利到达肿瘤微环境中发挥作用。
 
目前一个比较好的方法是结合CD47阻断与其它抗肿瘤药物进行结合治疗。比如anti-CD40抗体可以用于激活APC,特异性的抗肿瘤药物,以及FDA批准的免疫检查点单抗,Anti-CTLA-4,anti-PD-1等等。

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原文出处:

Xiaojuan Liu,Yang Pu,Kyle Cron,et.al.CD47 blockade triggers T cell-mediated destruction of immunogenic tumors nat med.2015
 

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    2015-11-09 liye789132251
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    2016-06-25 qidongfanjian
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    2015-11-13 kalseyzl
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