iNKT Cells Control Mouse Spontaneous Carcinoma Independently of Tumor-Specific Cytotoxic T Cells
Author(s) -
Matteo Bellone,
Monica Ceccon,
Matteo Grioni,
Elena Jachetti,
Arianna Calcinotto,
Anpolitano,
Massimo Freschi,
Giulia Casorati,
Paolo Dellabona
Publication year - 2010
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0008646
Subject(s) - cytotoxic t cell , immune system , ctl* , biology , tramp , immunology , cancer research , cd1d , carcinogenesis , acquired immune system , genetically modified mouse , natural killer t cell , cancer , adenocarcinoma , t cell , transgene , cd8 , biochemistry , genetics , gene , in vitro
Background CD1d-restricted invariant NKT (iNKT) cells are a subset of T lymphocytes endowed with innate effector functions that aid in the establishment of adaptive T and B cell immune responses. iNKT cells have been shown to play a spontaneous protective role against experimental tumors. Yet, the interplay between iNKT and tumor-specific T cells in cancer immune surveillance/editing has never been addressed. The transgenic adenocarcinoma of the mouse prostate (TRAMP) is a realistic model of spontaneous oncogenesis, in which the tumor-specific cytotoxic T cell (CTL) response undergoes full tolerance upon disease progression. Principal Findings We report here that lack of iNKT cells in TRAMP mice resulted in the appearance of more precocious and aggressive tumors that significantly reduced animal survival. TRAMP mice bearing or lacking iNKT cells responded similarly to a tumor-specific vaccination and developed tolerance to a tumor-associated antigen at comparable rate. Conclusions Hence, our data argue for a critical role of iNKT cells in the immune surveillance of carcinoma that is independent of tumor-specific CTL.
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