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Journal of Immunology Research
Volume 2017 (2017), Article ID 2471627, 7 pages
https://doi.org/10.1155/2017/2471627
Research Article

Antitumor Effect of KML-B-Treated Dendritic Cells via Induction of Lymphocyte Activation

1Singapore Bioimaging Consortium, Agency for Science, Technology and Research, 11 Biopolis Way, No. 02-02 Helios, Singapore 138667
2Department of Pharmacy, Sunchon National University, 255 Jungangno, Suncheon 540-950, Republic of Korea
3Mistle Biotech Co. Ltd, Pohang 37668, Republic of Korea
4Department of Hematology-Oncology, Chonnam National University Hwasun Hospital, Hwasun 519-763, Republic of Korea
5Suncheon Research Center for Natural Medicines, Suncheon, Republic of Korea

Correspondence should be addressed to Sung-Tae Yee; rk.ca.nohcnus@eatgnus

Received 11 November 2016; Revised 6 February 2017; Accepted 5 March 2017; Published 29 May 2017

Academic Editor: Ramon Kaneno

Copyright © 2017 Jong-Jin Kim et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Lectins are carbohydrate-binding proteins with various biological activities, such as antitumor and immunomodulatory effects. Although lectins have various biological activities, they are still limited by cytotoxicity in normal cells. To overcome this problem, we used the noncytotoxic part of Korean mistletoe lectin B-chain (KML-B) to induce maturation of dendritic cells (DCs). A previous study reported that KML-B induces DC maturation by triggering TLR-4, including expression of costimulatory molecules (CD40, CD80, and CD86), MHC II, and secretion of cytokines in DCs. Additionally, matured DCs by KML-B induced T helper (Th) cell activation and differentiation toward Th1 cells. However, the interaction of KML-B-treated DCs with CD8+ T cells is still poorly understood. In this study, we confirmed the ability of matured DCs by KML-B to stimulate cytotoxic T cells using OT-1 mouse-derived CD8+ T cells. KML-B induced MHC I expression in DCs, stimulation of CD8+ T cell activation and proliferation, and IFN-γ secretion. Moreover, tumor sizes were reduced by KML-B treatment during vaccination of OVA257−264-pulsed DCs. Here, we confirmed induction of CD8+ T cell activation and the antitumor effect of KML-B treatment in DCs.