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. 2015 Apr 1;4(8):e1021538. doi: 10.1080/2162402X.2015.1021538

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© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

©Heleen H Van Acker, Sébastien Anguille, Viggo F Van Tendeloo, and Eva Lion

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License http://creativecommons.org/licenses/by-nc/3.0/, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 1. — How γδ T cells can contribute to the antitumor efficacy of dendritic cell (DC)-based vaccination. It can be postulated that DC vaccination has the ability to activate γδ T cells and initiate their expansion. In turn, activated γδ T cells can (I) further stimulate vaccine and host DCs indirectly supporting sustained antitumor T-cell immunity and NK-DC crosstalk, (II) fulfil their immunomodulatory function through the secretion of pro-inflammatory cytokines regulating innate (natural killer cells) and adaptive (T cells) cellular immunity, and (III) directly kill tumor cells. Abbreviations: CTL, cytotoxic T lymphocyte; DC, dendritic cell; DNAM, DNAX accessory molecule; FASL, Fas ligand; IFN, interferon; IL, interleukin; IPP, isopentenyl pyrophosphate; NK, natural killer cells; TC, tumor cell; TCR, tumor cell; Th1, T-helper 1 cell; TNF, tumor necrosis factor; TRAIL, TNF-related apoptosis-inducing ligand.