PD-1 blockade enhances cytokine-induced killer cell-mediated cytotoxicity in B-cell non-Hodgkin lymphoma cell lines.

Autor: Li Y; Department of Integrated Oncology (CIO), University Hospital Bonn, D-53127 Bonn, Germany., Sharma A; Department of Integrated Oncology (CIO), University Hospital Bonn, D-53127 Bonn, Germany.; Department of Neurosurgery, University Hospital Bonn, D-53127 Bonn, Germany., Bloemendal MWJR; Department of Biosciences, Hogeschool van Arnhem en Nijmegen University of Applied Sciences, 6525EM Nijmegen, The Netherlands., Schmidt-Wolf R; Department of Anesthesiology and Intensive Care Medicine, University Hospital Bonn, D-53127 Bonn, Germany., Kornek M; Department of Medicine I, University Hospital Bonn, D-53127 Bonn, Germany., Schmidt-Wolf IGH; Department of Integrated Oncology (CIO), University Hospital Bonn, D-53127 Bonn, Germany.
Jazyk: angličtina
Zdroj: Oncology letters [Oncol Lett] 2021 Aug; Vol. 22 (2), pp. 613. Date of Electronic Publication: 2021 Jun 23.
DOI: 10.3892/ol.2021.12874
Abstrakt: 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.
Competing Interests: The authors declare that they have no competing interests.
(Copyright: © Li et al.)
Databáze: MEDLINE
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