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. 2019 Dec 11;10:2766. doi: 10.3389/fimmu.2019.02766

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Copyright © 2019 Wickström, Lövgren, Volkmar, Reinhold, Duke-Cohan, Hartmann, Rebmann, Mueller, Melief, Maas, Ligtenberg, Hansson, Offringa, Seliger, Poschke, Reinherz and Kiessling.

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) and the copyright owner(s) 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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Recognition of autologous tumor cells or peptides from shared tumor-associated antigens, from mutated genes, or from viruses by tumor-infiltrating lymphocytes. Tumor-infiltrating lymphocytes (TIL) and primary tumor cell lines were expanded from tumors of patients KADA and ANRU. The ability of TIL to recognize corresponding tumor cells or HLA-A2-transfected SK-OV-3 target cells pulsed with peptides from common tumor-associated antigens or viruses (A, KADA; D, ANRU), or HLA-A2-transfected SK-OV-3 cells pulsed with neoepitope peptides derived from mutated genes in tumor cells, in the absence or presence of anti-HLA-A2 (BB7.4) or -MHC-I (W6/32) blocking monoclonal antibodies (B, KADA; E, ANRU; only recognized peptides shown), or HLA-A2-transfected SK-OV-3 pulsed with neoepitope peptides compared to corresponding wild-type peptides (C, KADA; F, ANRU), and respond with IFN-γ secretion was assessed after 24 h by ELISA. Unpulsed HLA-A2-transfected SK-OV-3 target cells were used as a no peptide control and pulsed original SK-OV-3 cells (Ctrl) were used as a no HLA-A2 control as indicated.