Cytokines for the induction of antitumor effectors: The paradigm of Cytokine-Induced Killer (CIK) cells
Cytokines for the induction of antitumor effectors: The paradigm of Cytokine-Induced Killer (CIK) cells
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DOI：
10.1016/j.cytogfr.2017.06.003
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发表时间：
2017-08-01
影响因子：
13
通讯作者：
Rosato, Antonio
中科院分区：
文献类型：
--
作者：
Cappuzzello, Elisa;Sommaggio, Roberta;Rosato, Antonio
细胞因子诱导杀伤（CIK）细胞正引起人们对细胞抗肿瘤治疗越来越多的兴趣，因为它们可以通过简单而廉价的方案轻松扩展，并且只需要gmp级细胞因子就可以获得大量的细胞毒性细胞。CIK细胞不需要抗原特异性刺激来激活和增殖，因为它们通过NKG2D的参与以不依赖hla的方式识别和破坏肿瘤细胞。在一些临床前研究和临床试验中，与传统T细胞相比，CIK细胞表现出较低的同种异体反应性，即使在跨越hla屏障的情况下也是如此；只有少数患者在接受同种异体CIK细胞治疗后出现轻度GVHD。此外，它们的抗肿瘤活性可以通过嵌合抗原受体、临床级单克隆抗体或免疫检查点抑制剂重新定向和进一步提高。从越来越多的文献中获得的证据支持CIK细胞是一种非常有前途的过继免疫治疗细胞群。在这篇综述中，所有这些方面将特别强调细胞因子在CIK细胞产生、扩增和功能化中的作用。(C) 2017年作者。Elsevier Ltd.出版。这是一篇基于CC BY-NC-ND许可（http://creativecommons.org/licenses/by-nc-nd/4.0/）的开放获取文章。
Cytokine-Induced killer (CIK) cells are raising growing interest in cellular antitumor therapy, as they can be easily expanded with a straightforward and inexpensive protocol, and are safe requiring only GMP-grade cytokines to obtain very high amounts of cytotoxic cells. CIK cells do not need antigen-specific stimuli to be activated and proliferate, as they recognize and destroy tumor cells in an HLA-independent fashion through the engagement of NKG2D. In several preclinical studies and clinical trials, CIK cells showed a reduced alloreactivity compared to conventional T cells, even when challenged across HLA-barriers; only in a few patients, a mild GVHD occurred after treatment with allogeneic CIK cells. Additionally, their antitumor activity can be redirected and further improved with chimeric antigen receptors, clinical-grade monoclonal antibodies or immune checkpoint inhibitors. The evidence obtained from a growing body of literature support CIK cells as a very promising cell population for adoptive immunotherapy. In this review, all these aspects will be addressed with a particular emphasis on the role of the cytokines involved in CIK cell generation, expansion and functionalization. (C) 2017 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).