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Antitumor effects and mechanisms of dendritic cells stimulated by sCD40L on ovarian cancer cells in vitro
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Authors: Zhang ZM, Yang XM, Zhang C, Zhang MJ, Li X, Zhang FH, Kang S, Wang SJ, Shan BE
Published Date May 2013
Volume 2013:6 Pages 503 - 515
|Received:||19 November 2012|
|Accepted:||04 February 2013|
|Published:||06 May 2013|
1Department of Gynecology and Obstetrics, Fourth Hospital of Hebei Medical University, 2Research Center, Fourth Hospital of Hebei Medical University, 3Department of General Surgery, Hebei General Hospital, 4Department of Gastroscopy, Fourth Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China
Objective: This study aimed to examine the expression of immune suppression factors and the mechanisms of antitumor effects of cord blood dendritic cells (DCs) stimulated by soluble cluster of differentiation 40 ligand (sCD40L) and cytokines in vitro in ovarian cancer patients.
Methods: The expression levels of interleukin (IL)-10 and transforming growth factor (TGF)-β messenger RNA in peripheral blood were detected by reverse transcription polymerase chain reaction; expression levels of CD80 and CD86 in DCs stimulated by sCD40L were detected using flow cytometry and confocal laser scanning microscopy.
Results: Expression levels of IL-10 and TGF-β genes in the peripheral blood of ovarian cancer patients were significantly increased compared with patients with benign ovarian tumors (P < 0.05). The expression levels of CD80 and CD86 in DCs cultured in the granulocyte-macrophage colony-stimulating factor + IL-4 + stem cell factor + Flt-3 ligand + sCD40L group were significantly increased compared with those in the control group, as assessed by flow cytometry and confocal laser scanning microscopy (P < 0.05).
Conclusion: A variety of cytokines in combination with sCD40L can promote the proliferation of cord blood-derived DCs and induce their maturation as well as stimulating a specific antitumor response.
Keywords: antitumor response, cytokine, immunotherapy, cord blood, IL-10, TGF-β
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