Department of Oncological Sciences, Laboratory of Cell Therapy of Cancer, University of Torino Medical School, Institute for Cancer Research and Treatment, Candiolo, Torino, Italy.
J Immunother. 2012 Sep;35(7):579-86. doi: 10.1097/CJI.0b013e31826b1fd9.
Cytokine-induced killer cells (CIKs) are ex vivo expanded T-NK lymphocytes capable of HLA-unrestricted antitumor activity. CIKs are promising candidates for adoptive cancer immunotherapies; they can be generated and infused in autologous settings of cancer patients, or from donors, after allogeneic hematopoietic cell transplant. Ex vivo expansion rates of CIKs are greatly variable among patients, with consequent potential clinical limitations for "poor expanders." We compared the standard expansion protocol with a new one, which included the timed addition of irradiated allogeneic peripheral blood mononuclear cells. Our hypothesis is that allogeneic stimulation might provide CIK cells with a proliferative boost and simultaneously decrease their alloreactivity versus third parties, if HLA-mismatched from the allogeneic stimulators. Allo-stimulated CIKs (AS-CIK) reached significantly higher expansion rates compared with standard controls, regardless if generated form healthy donors (131- vs. 32-fold) or cancer patients (117- vs. 14-fold). The expansion of the CD3CD56 subset was 2243-fold for AS-CIKs compared with 362 for standard CIKs. AS-CIKs efficiently killed osteosarcoma targets in vitro, results were comparable with that of standard CIKs. Standard and AS-CIKs did not show differences in phenotype and telomere length. The alloreactivity of AS-CIKs against third party HLA-mismatched peripheral blood mononuclear cells was reduced compared with standard CIKs (37% vs. 23%). In conclusion, alloreactivity of CIK cells may be exploited enhancing their final ex vivo expansion. In clinical perspective these findings may facilitate the extension of CIK-based immunotherapy to larger numbers of patients and, translated into hematopoietic cell transplant settings, contribute to reduce the risk of graft versus host disease in the hypothesis of infusions across HLA barriers.
细胞因子诱导的杀伤细胞(CIKs)是体外扩增的 T-NK 淋巴细胞,能够进行 HLA 非限制性抗肿瘤活性。CIKs 是过继性癌症免疫疗法的有前途的候选者;它们可以在癌症患者的自体环境中生成和输注,也可以在异基因造血细胞移植后从供体中生成和输注。CIKs 的体外扩增率在患者之间差异很大,因此对于“扩增不良者”存在潜在的临床限制。我们比较了标准扩增方案和一种新方案,该方案包括定时添加辐照的异体外周血单个核细胞。我们的假设是,同种异体刺激可能会为 CIK 细胞提供增殖促进作用,同时降低其对第三方的同种异体反应性,如果与同种异体刺激剂的 HLA 不匹配的话。与标准对照相比,同种刺激的 CIK 细胞(AS-CIK)达到了更高的扩增率,无论它们是由健康供体(131 倍与 32 倍)还是癌症患者(117 倍与 14 倍)产生的。与标准 CIK 相比,AS-CIK 的 CD3CD56 亚群扩增了 2243 倍。AS-CIK 能够有效地在体外杀伤骨肉瘤靶细胞,结果与标准 CIK 相当。标准和 AS-CIK 在表型和端粒长度方面没有差异。与标准 CIK 相比,AS-CIK 对第三方 HLA 错配的外周血单个核细胞的同种异体反应性降低(37%与 23%)。总之,CIK 细胞的同种异体反应性可以通过增强其最终的体外扩增来利用。从临床角度来看,这些发现可能有助于将基于 CIK 的免疫疗法扩展到更多的患者,并在假设 HLA 障碍下输注的情况下,有助于降低移植物抗宿主病的风险,转化为造血细胞移植环境。
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