In vivo and in vitro killing activity of CIK cells plus L-OHP on OCUM-2MD3/L-OHP cells Previous studies have shown that the overexpression of P-gp in MDR tumor cells enhances the immunogenicity

of target cells, and makes the target cells more easily be recognized by immune effector cells. Therefore, the cytotoxic effect of immune effector cells see more against drug-resistant tumor cells was similar or even stronger than against parental cells. Moreover, maintenance of in vivo cytotoxicity against tumor cells was not necessarily dependent on the sustained administration of large doses of exogenous interleukin (IL)-2 [16, 33–35]. Application of immunocytes, including CIK cells, may be a feasible treatment for drug-resistant tumors, although MGCD0103 cell line this treatment requires further investigation. This study indicates that CIK cells manifeste stronger in vitro killing activity against drug-resistant cells than against parental cells. The possible mechanism underlying this phenomenon may be the CD3+CD56+ double positive cells as cytoplasmic particles to kill tumor cells released when CIK cells are stimulated. Additionally, a large amount of inflammatory cytokines, such as TNF-α, IL-2 and GM-CSF, are released by the activated

CIK cells, which can directly inhibit tumor cells, or indirectly kill tumor cells by modulating the immune system. Previous studies suggested that CIK cells play a critical role in the accumulation of chemotherapeutic 17-DMAG (Alvespimycin) HCl drugs in MDR tumor cells, and that the killing activity of CIK cells plus chemotherapeutic drugs against MDR tumor cells was significantly higher than with chemotherapeutic drugs along. Furthermore, the killing activity of CIK cells is proportional to the ratio of

effector cells to target cells. However, the in vivo killing activity cannot be accurately measured [10]. Lack of this knowledge may result in unsatisfactory immune therapeutic LY3023414 supplier effects in certain patients. The combination of immune effector cells and chemotherapeutic drugs against MDR target cells was able to improve the sensitivity of drug-resistant cells to chemotherapeutic drugs. This dual treatment showed excellent effects in scavenging remnant tumor cells expressing drug-resistant proteins in postoperative patients, even in drug-resistant tumors in middle and advanced stages irresponsible to radiotherapy and chemotherapy. Our study revealed that the in vivo and in vitro killing activity of CIK cells combined with various concentrations of L-OHP against two types of tumor cells was significantly enhanced in comparison with the use of L-OHP or CIK cells alone. Moreover, the killing activity of CIK cells combined with L-OHP against drug-resistant cells showed stronger synergetic effects than the similar treatment of parental cells, providing evidence of improved anti-tumor effects for the clinical application of CIK cells combined with L-OHP.