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. 2018 Jan 25;8:1975. doi: 10.3389/fimmu.2017.01975

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Copyright © 2018 Khan, Carmona, Sukhumalchandra, Roszik, Philips, Perakis, Kerros, Zhang, Qiao, John, Zope, Goldberg, Qazilbash, Jakher, Clise-Dwyer, Qiu, Mittendorf, Molldrem, Kornblau and Alatrash.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ALL shows susceptibility to killing by CG1-cytotoxic T lymphocytes (CTLs). Patient samples (UPN2, UPN5 and UPN7), T2 cells, and Raji-A2 cells were loaded with calcein-AM, and then cocultured with CG1-CTLs for 4 h at various E (effector): T (target) ratios. Cytotoxicity was determined by measurement of intracellular calcein-AM in live cells. T2 cell lines were pulsed with CG1 and E75 peptide as positive and negative controls, respectively. (A) UPN7, which endogenously expresses Cathepsin G (CG), and (B) Raji-A2 pulsed with purified CG protein (see Figure S5 in Supplementary Material) showed increased killing by CG1-CTL. Cytotoxicity data are means ± SEM from triplicate wells from a representative experiment. *P < 0.05; **P < 0.01; ***P < 0.001.