METHODS: CIK cells consist of CD3+/CD56+ natural killer (NK) T cells, CD3-/CD56+ NK cells, and CD3+/CD56- cytotoxic T cells. In this regard, the CD3+/CD56+ NK T cells are the primary effectors. Compared with the previously reported antitumor immune cells, CIK cells are characterized by improved in vitro proliferation and amplification, enhanced migration and invasive capacity to tumor region, more significant antitumor activity, and a broader antitumor spectrum. CIK cells can also induce death in tumor cells via numerous pathways and mechanisms. Hence, CIKs-based therapy has been used in various clinical trials and has shown efficacy with a very low graft versus host disease (GVHD) against several cancers, such as hematologic malignancies, even in relapsing cases, or cases not responding to other therapies. Despite the high content of T cells, CIK cells induce low alloreactivity and, thus, pose a restricted threat of GVHD induction even in MHC-mismatched transplantation cases. Phase 1 and 2 clinical trials of CIK cell therapy have also highlighted satisfactory therapeutic advantages against hematologic cancers, indicating the safety of CIK cells even in haploidentical transplantation settings.
CONCLUSIONS: CIK cells have shown promising results in the treatment of hematologic malignancies, especially in combination with other antitumor strategies. However, the existing controversies in achieving desired clinical responses underscore the importance of future studies.
方法:CIK细胞由CD3+/CD56+自然杀伤(NK)T细胞组成,CD3-/CD56+NK细胞,和CD3+/CD56-细胞毒性T细胞。在这方面,CD3+/CD56+NKT细胞是主要效应子。与以前报道的抗肿瘤免疫细胞相比,CIK细胞的特点是体外增殖和扩增得到改善,增强了对肿瘤区域的迁移和侵袭能力,更显著的抗肿瘤活性,和更广泛的抗肿瘤谱。CIK细胞还可以通过多种途径和机制诱导肿瘤细胞死亡。因此,基于CIKs的治疗已被用于各种临床试验,并已显示出对几种癌症的非常低的移植物抗宿主病(GVHD)的疗效。比如血液系统恶性肿瘤,即使在复发病例中,或对其他疗法无反应的病例。尽管T细胞含量高,CIK细胞诱导低同种异体反应性,因此,即使在MHC不匹配的移植病例中,也会对GVHD诱导产生有限的威胁。CIK细胞疗法的1期和2期临床试验也突出了对血液系统癌症的令人满意的治疗优势。表明即使在单倍体相同的移植环境中,CIK细胞也是安全的。
结论:CIK细胞在血液系统恶性肿瘤的治疗中显示了有希望的结果,特别是与其他抗肿瘤策略相结合。然而,在达到预期临床反应方面存在的争议强调了未来研究的重要性.