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Involvement of CD166 in the Activation of Human T Cells by Tumor Cells Sensitized with Nonpeptide Antigens¹

Yu Kato^*, Yoshimasa Tanaka^*,, Mikihito Hayashi^*, Katsuya Okawa and Nagahiro Minato^2,*

^* Department of Immunology and Cell Biology, Graduate School of Biostudies, Kyoto University, Kyoto, Japan; Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, Saitama, Japan, and Horizontal Medical Research Organization, Kyoto University, Sakyo-Ku, Japan

We previously reported that human V2V2-T cells were activated by many human tumor cell lines treated with pamidronate (PAM) in a TCR-dependent manner. In the present study, we indicated that a synthetic pyrophosphomonoester Ag, 2-methy-3-butenyl-1-pyrophosphate, could directly "sensitize" the tumor cells to activate T cells independently of the host metabolism, while the sensitizing effect of PAM was reported to be dependent on the pharmacological activity. Some exceptional tumor cells that failed to be sensitized by PAM were incapable of activating T cells by the treatment with 2-methy-3-butenyl-1-pyrophosphate either, suggesting a requirement of host factor(s) for the effective T cell activation in addition to the nonpeptide Ags. By screening mAbs against a large panel of tumor cell lines, we found that the expression of CD166 closely paralleled the capacity of activating T cells upon PAM treatment. The transfection of a CD166-negative tumor cell line with CD166 cDNA caused a marked enhancement of the capacity to activate T cells following PAM treatment. On the contrary, down-regulation of the CD166 expression in a CD166-bearing tumor cell line by short hairpin RNA resulted in a significant reduction of PAM-induced T cell-stimulatory activity. T cells expressed CD6, a receptor of CD166, and CD6 and CD166 were recruited together to the center of synapse between T cells and PAM-treated tumor cells, colocalizing with TCR/CD3. The results suggested that the engagement of CD6 with CD166 on tumor cells played an important role in the T cell activation by the tumor cells loaded with nonpeptide Ags either endogenously or exogenously.

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