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. 2015 Apr 27;5(1):e1025194. doi: 10.1080/2162402X.2015.1025194

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© The Author(s). Published with license by Taylor & Francis

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted 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 3. — (A) Killing of wild-type Ewing's sarcoma cell lines by expanded Vδ2+ γδT cells opsonized with ch14.18/CHO anti-GD2 antibody or in the presence of a control antibody (Rituximab) (n = 3–6, **p = 0.0099). (B) Killing of isogenic GD2^bright and GD2^dim DC-ES6 Ewing's cell lines by Vδ2+ γδT cells in the presence of ch14.18/CHO anti-GD2 opsonizing antibody or Rituximab control antibody (n = 3, ***p = 0.0033). (C) IFNγ expression of Vδ2+ γδT cells in the presence of GD2^bright DC-ES6. Elimination of the DC-ES6 population and production of IFNγ is only seen when DC-ES6 is opsonized with ch14.18/CHO. (D) Correlation between the GD2 stain (PE-SFI) of Ewing's sarcoma and neuroblastoma cell lines and the degree to which Vδ2+ γδT cells exert ADCC or AIC against them at effector:target ratio 10:1. R value calculated by Spearman correlation.