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Blood, 15 February 2006, Vol. 107, No. 4, pp. 1491-1496.
Prepublished online as a Blood First Edition Paper on October 25, 2005; DOI 10.1182/blood-2005-04-1684.
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IMMUNOBIOLOGY
Tumor rejection by the poliovirus receptor family ligands of the DNAM-1 (CD226) receptor
Satoko Tahara-Hanaoka,
Kazuko Shibuya,
Hirayasu Kai,
Akitomo Miyamoto,
Yoshihiro Morikawa,
Nobuhiro Ohkochi,
Shin-ichiro Honda, and
Akira Shibuya
From the Department of Immunology, Institute of Basic Medical Sciences and Center for Tsukuba Advanced Research Alliance (TARA); Department of Surgery, Institute of Clinical Medicine, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Ibaraki, Japan; Subteam for Manipulation of Cell Fate, BioResource Center, RIKEN Tsukuba Institute, Ibaraki, Japan; and Department of Anatomy and Neurobiology, Wakayama Medical University, Wakayama, Japan.
The poliovirus receptor CD155 and its family member CD112 (nectin-2) are the ligands for the activating cell-surface receptor DNAM-1 on CD8+ T cells and natural killer (NK) cells. Here, we demonstrate that, whereas the RMA tumor grew in syngeneic mice, DNAM-1 ligand-transduced RMA was rejected, in which CD8+ T cells and NK cells played an essential role. Importantly, CD8+ memory cytotoxic T cells to parental RMA were generated in these mice. We found that DNAM-1 was also expressed on CD8 +, rather than CD8-, dendritic cells (DCs). Cross-linking DNAM-1 induced maturation of CD8+ DCs. Antigen presentation by these stimulated DCs drove Th1 cells. Moreover, the rejection of DNAM-1 ligand-transduced RMA was canceled in CD4+ T-cell–depleted and major histocompatibility complex class II–deficient mice. Taken together, these results suggest that DNAM-1 ligands stimulate innate immunity by CD8+ DCs as well as NK cells, which efficiently prime cell-mediated tumor-specific immunity.
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