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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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Submitted May 5, 2005
Accepted October 6, 2005
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*
Department of Immunology, Institute of Basic Medical Sciences and Center for TARA, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba-city, Ibaraki, Japan
Department of Immunology, Institute of Basic Medical Sciences and Center for TARA, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba-city, Ibaraki, Japan; Subteam for Manipulation of Cell Fate, BioResource Center, RIKEN Tsukuba Institute, Tsukuba-city, Ibaraki, Japan
Department of Anatomy and Neurobiology, Wakayama Medical University, Wakayama, Japan
Department of Surgery, Institute of Clinical Medicine, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba-city, Ibaraki, Japan
* Corresponding author; email: ashibuya{at}md.tsukuba.ac.jp.
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 NK cells. Here, we demonstrated that, while the RMA tumor grew in syngenic mice, DNAM-1 ligands-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. Cross-linking DNAM-1 induced maturation of CD8+ dendritic cells. Antigen presentation by these stimulated dendritic cells drived Th1 cells. Moreover, the rejection of DNAM-1 ligands-transduced RMA was canceled in CD4+ T cell-depleted and MHC class II deficient mice. Taken together, these results suggest that DNAM-1 ligands stimulate innate immunity by CD8+ dendritic cells as well as NK cells, which efficiently prime cell-mediated tumor specific immunity.
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