TY - JOUR
T1 - Oncolytic viruses sensitize human tumor cells for NY-ESO-1 tumor antigen recognition by CD4+ effector T cells
AU - Delaunay, Tiphaine
AU - Violland, Mathilde
AU - Boisgerault, Nicolas
AU - Dutoit, Soizic
AU - Vignard, Virginie
AU - Münz, Christian
AU - Gannage, Monique
AU - Dréno, Brigitte
AU - Vaivode, Kristine
AU - Pjanova, Dace
AU - Labarrière, Nathalie
AU - Wang, Yaohe
AU - Chiocca, E. Antonio
AU - Boeuf, Fabrice Le
AU - Bell, John C.
AU - Erbs, Philippe
AU - Tangy, Frédéric
AU - Grégoire, Marc
AU - Fonteneau, Jean François
N1 - Funding Information:
This work was supported by ?La Ligue R?gionale Grand Ouest contre le Cancer? (CSIRGO: CD16, CD22, CD44, CD49, CD72, CD79 and CD85), ?La Ligue Nationale contre le Cancer?, ? l'association ARSMESO44 ?, ?La Fondation du Souffle et le Fonds de Dotation Recherche en Sant? Respiratoire?, ?La fondation ARC?, ?la Fondation pour la Recherche M?dicale (FRM)?, Agence Nationale pour la Recherche (ANR-16-CE18-0016) and LabEX IGO program supported by the National Research Agency via the investment of the future program ANR-11-LABX-0016-01?. JCB is supported by the Canadian Cancer Society, the Terry Fox Foundation and the Ontario Institute for Cancer research. We thank Philippe Hulin and the cellular and tissular core facility of Nantes University (MicroPiCell) for their expertise in video microscopy. We thank Juliette Desfran?ois and the core facility of flow cytometry (Cytocell).
Funding Information:
This work was supported by “La Ligue Régionale Grand Ouest contre le Cancer” (CSIRGO: CD16, CD22, CD44, CD49, CD72, CD79 and CD85), “La Ligue Nationale contre le Cancer”, “ l’association ARSMESO44 ”, “La Fondation du Souffle et le Fonds de Dotation Recherche en SantéRespira-toire”, “La fondation ARC”, “la Fondation pour la Recherche Médicale (FRM)”, Agence Nationale pour la Recherche (ANR-16-CE18-0016) and LabEX IGO program supported by the National Research Agency via the investment of the future program ANR-11-LABX-0016-01”. JCB is supported by the Canadian Cancer Society, the Terry Fox Foundation and the Ontario Institute for Cancer research.
Publisher Copyright:
© 2018 Taylor & Francis Group, LLC.
PY - 2018/3/4
Y1 - 2018/3/4
N2 - Oncolytic immunotherapy using oncolytic viruses (OV) has been shown to stimulate the antitumor immune response by inducing the release of tumor-associated antigens (TAA) and danger signals from the dying infected tumor cells. In this study, we sought to determine if the lysis of tumor cells induced by different OV: measles virus, vaccinia virus, vesicular stomatitis virus, herpes simplex type I virus, adenovirus or enterovirus, has consequences on the capacity of tumor cells to present TAA, such as NY-ESO-1. We show that the co-culture of NY-ESO-1neg/HLA-DP4pos melanoma cells with NY-ESO-1pos/HLA-DP4neg melanoma cells infected and killed by different OV induces an intercellular transfer of NY-ESO-1 that allows the recognition of NY-ESO-1neg/HLA-DP4pos tumor cells by an HLA-DP4/NY-ESO-1(157–170)-specific CD4+ cytotoxic T cell clone, NY67. We then confirmed this result in a second model with an HLA-DP4+ melanoma cell line that expresses a low amount of NY-ESO-1. Recognition of this cell line by the NY67 clone is largely increased in the presence of OV productive infection. Altogether, our results show for the first time another mechanism of stimulation of the anti-tumor immune response by OV, via the loading of tumor cells with TAA that sensitizes them for direct recognition by specific effector CD4+ T cells, supporting the use of OV for cancer immunotherapy.
AB - Oncolytic immunotherapy using oncolytic viruses (OV) has been shown to stimulate the antitumor immune response by inducing the release of tumor-associated antigens (TAA) and danger signals from the dying infected tumor cells. In this study, we sought to determine if the lysis of tumor cells induced by different OV: measles virus, vaccinia virus, vesicular stomatitis virus, herpes simplex type I virus, adenovirus or enterovirus, has consequences on the capacity of tumor cells to present TAA, such as NY-ESO-1. We show that the co-culture of NY-ESO-1neg/HLA-DP4pos melanoma cells with NY-ESO-1pos/HLA-DP4neg melanoma cells infected and killed by different OV induces an intercellular transfer of NY-ESO-1 that allows the recognition of NY-ESO-1neg/HLA-DP4pos tumor cells by an HLA-DP4/NY-ESO-1(157–170)-specific CD4+ cytotoxic T cell clone, NY67. We then confirmed this result in a second model with an HLA-DP4+ melanoma cell line that expresses a low amount of NY-ESO-1. Recognition of this cell line by the NY67 clone is largely increased in the presence of OV productive infection. Altogether, our results show for the first time another mechanism of stimulation of the anti-tumor immune response by OV, via the loading of tumor cells with TAA that sensitizes them for direct recognition by specific effector CD4+ T cells, supporting the use of OV for cancer immunotherapy.
KW - CD4+ T Lymphocytes
KW - Melanoma
KW - Oncolytic immunotherapy
KW - Oncolytic Viruses
KW - Tumor-Associated Antigens
UR - http://www.scopus.com/inward/record.url?scp=85039034040&partnerID=8YFLogxK
U2 - 10.1080/2162402X.2017.1407897
DO - 10.1080/2162402X.2017.1407897
M3 - Article
C2 - 29399408
AN - SCOPUS:85039034040
SN - 2162-4011
VL - 7
JO - OncoImmunology
JF - OncoImmunology
IS - 3
M1 - e1407897
ER -
