Newly emerged immunogenic neoantigens in established tumors enable hosts to regain immunosurveillance in a T-cell-dependent manner.


Journal

International immunology
ISSN: 1460-2377
Titre abrégé: Int Immunol
Pays: England
ID NLM: 8916182

Informations de publication

Date de publication:
01 01 2021
Historique:
received: 17 06 2020
accepted: 25 07 2020
pubmed: 31 7 2020
medline: 10 2 2022
entrez: 31 7 2020
Statut: ppublish

Résumé

Tumor neoantigens derived from genetic alterations are potential T-cell targets for antitumor immunity. However, tumors develop immune escape mechanisms including loss of preexisting neoantigens and/or impairment of T-cell responses during tumor development and progression. Here, we addressed whether newly emerged immunogenic neoantigens in established tumors enabled hosts to inhibit tumor growth via controlling immune escape mechanisms. Using a doxycycline-driven gene expression system, we generated murine MC38, CT26 (colorectal cancer) and B16 (melanoma) cell lines with inducible expression of model immunogenic neoantigens such as chicken ovalbumin and human NY-ESO-1. A model neoantigen was induced by doxycycline administration in the tumors once tumors became palpable. Tumor growth was significantly inhibited upon induction of the neoantigen and this inhibition was abrogated in nude mice lacking T cells and in mice deprived of CD8+ T cells, indicating the critical role of CD8+ T cells in tumor regression. In addition, PD-1/PD-L1 blockade further augmented the antitumor immune response, resulting in a far stronger inhibition of tumor growth. Accordingly, newly emerged tumor neoantigen-specific CD8+ T cells with enhanced effector functions were significantly increased in mice treated with PD-1/PD-L1 blockade. We propose that a newly emerged neoantigen is sufficient to inhibit tumor growth via preventing immune escape in a T-cell-dependent manner. Our results imply that induction of immunogenic tumor neoantigens is a novel strategy to overcome the resistance to immune checkpoint blockade therapy.

Identifiants

pubmed: 32729901
pii: 5878926
doi: 10.1093/intimm/dxaa049
doi:

Substances chimiques

Antigens, Neoplasm 0
B7-H1 Antigen 0
CTAG1B protein, human 0
Cd274 protein, mouse 0
Immune Checkpoint Inhibitors 0
Membrane Proteins 0
Pdcd1 protein, mouse 0
Programmed Cell Death 1 Receptor 0
Ovalbumin 9006-59-1
Doxycycline N12000U13O

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

39-48

Informations de copyright

© The Japanese Society for Immunology. 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Auteurs

Tomoaki Muramatsu (T)

Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Department of Urology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Takuro Noguchi (T)

Department of Medical Oncology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Daisuke Sugiyama (D)

Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Yoshie Kanada (Y)

Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Department of Urology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Kaori Fujimaki (K)

Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Sachiko Ito (S)

Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Momokazu Gotoh (M)

Department of Urology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Hiroyoshi Nishikawa (H)

Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Division of Cancer Immunology, Research Institute, National Cancer Center, Tokyo, Japan.
Division of Cancer Immunology, Exploratory Oncology Research and Clinical Trial Center (EPOC), National Cancer Center, Chiba, Japan.

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Classifications MeSH