OBJECTIVE This article is to verify feasibility and validity of autologous cytokine-induced killer cell (Auto-CIK) treatment in solid malignancypatients.METHODS Amplification, phenotypic characteristics, cytokine secr...OBJECTIVE This article is to verify feasibility and validity of autologous cytokine-induced killer cell (Auto-CIK) treatment in solid malignancypatients.METHODS Amplification, phenotypic characteristics, cytokine secretion,antitumor cytotoxicity and clinical response to Auto-CIK derived from 65cases of solid tumor patients with different pathological types and clinicalstages were compared with LAKs in a large-scale clinical trial,RESUL'r$ We found that seriousness of disease and metastatic status hadno influence on effective components and antitumor immunological activityof Auto-ClK. Comparing cytotoxicity against various tumor cells with LAKsat various effector to target ratios, ClKs showed more effective cytotoxicityagainst NK sensitive or non-sensitive solid tumor cell lines at a low E/T ratio(6:1) which suggests indirectly that Auto-CIK had a longer effective time invivo than LAKs. These results suggest that CIKs are more suitable forimmunotherapy for those solid malignancy patients at high risk of relapse orrecurrence.CONCLUSIONS Our experimental data were consistent ~ith the reportedconclusion that the potent antitumor activity of Auto-ClK mainly rooted in theCD4- part of CIKs, including CD3~CD56~ cells and CD8 ~ CTLs. The CD4~part of ClKs seemed to have no direct tumor lytic activity. The results indicatethat the special "Thl bias" and enhanced cytotoxicity against K562 cellsoccurred in PBMCs after multicycles of Auto-ClK infusions suggesting theinduction of a "Thl shift" and rectification of "Th2 dominance" in PBMC afterAuto-CIK treatments.展开更多
文摘OBJECTIVE This article is to verify feasibility and validity of autologous cytokine-induced killer cell (Auto-CIK) treatment in solid malignancypatients.METHODS Amplification, phenotypic characteristics, cytokine secretion,antitumor cytotoxicity and clinical response to Auto-CIK derived from 65cases of solid tumor patients with different pathological types and clinicalstages were compared with LAKs in a large-scale clinical trial,RESUL'r$ We found that seriousness of disease and metastatic status hadno influence on effective components and antitumor immunological activityof Auto-ClK. Comparing cytotoxicity against various tumor cells with LAKsat various effector to target ratios, ClKs showed more effective cytotoxicityagainst NK sensitive or non-sensitive solid tumor cell lines at a low E/T ratio(6:1) which suggests indirectly that Auto-CIK had a longer effective time invivo than LAKs. These results suggest that CIKs are more suitable forimmunotherapy for those solid malignancy patients at high risk of relapse orrecurrence.CONCLUSIONS Our experimental data were consistent ~ith the reportedconclusion that the potent antitumor activity of Auto-ClK mainly rooted in theCD4- part of CIKs, including CD3~CD56~ cells and CD8 ~ CTLs. The CD4~part of ClKs seemed to have no direct tumor lytic activity. The results indicatethat the special "Thl bias" and enhanced cytotoxicity against K562 cellsoccurred in PBMCs after multicycles of Auto-ClK infusions suggesting theinduction of a "Thl shift" and rectification of "Th2 dominance" in PBMC afterAuto-CIK treatments.
