PD‑1 blockade enhances cytokine‑induced killer cell‑mediated cytotoxicity in B‑cell non‑Hodgkin lymphoma cell lines
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- Published online on: June 23, 2021 https://doi.org/10.3892/ol.2021.12874
- Article Number: 613
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Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
The clinical utility of immune checkpoint inhibitors, such as programmed cell death protein 1 (PD‑1) and programmed death‑ligand 1 (PD‑L1) inhibitors used alone or in combination with other therapies, is currently gaining attention. In this particular scenario, the inclusion of cytokine‑induced killer (CIK) cells has proven to be a novel therapeutic approach. CIK cells have shown anticancer activity in various hematopoietic malignancies, but their defined cytotoxicity in B‑cell non‑Hodgkin lymphoma (B‑NHL) remains to be fully elucidated. The present study investigated the role of PD‑1/PD‑L1 blockades on the cytotoxic efficacy of CIK cells primarily in B‑NHL cell lines. The current analysis revealed that CIK cells prompted cytotoxicity against B‑NHL cell lines (DAUDI and SU‑DHL‑4), and a significant increase in PD‑L1 expression was observed when CIK cells were co‑cultured with B‑NHL cells. Additionally, a combination of PD‑1 and PD‑L1 antibodies with CIK cells significantly decreased cell viability only in DAUDI cells. Furthermore, IFN‑γ elevation was observed in both cell lines treated with CIK alone or with PD‑1 antibody, but this tendency was not observed for PD‑L1. Since PD‑1 can suppress immune inactivation, whereas CD40L can promote it, the effects of CD40L blockade were also examined; however, no significant changes in cell viability were observed. Overall, the present in vitro data suggested that CIK cells exerted a cytotoxic function in B‑NHL cells, and a combination of PD‑1 inhibitors with CIK cells may provide a potential therapeutic option for this type of lymphoma. Nevertheless, in vivo experiments are warranted to undermine the extent to which PD‑1 inhibitors may be used to enhance the antitumor activity of CIK cells in B‑NHL.
