コバヤシ　ヒロヒト   KOBAYASHI Hirohito   小林　博人    所属   医学部 医学科（附属足立医療センター）    職種   准教授
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Expression and function of PD-1 in human γδ T cells that recognize phosphoantigens.
掲載誌名	正式名：European journal of immunology 略　 称：Eur J Immunol ISSNコード：15214141/00142980
掲載区分	国外
巻・号・頁	41(2),pp.345-355
著者・共著者	Iwasaki Masashi, Tanaka Yoshimasa, Kobayashi Hirohito, Murata-Hirai Kaoru, Miyabe Hideto, Sugie Tomoharu, Toi Masakazu, Minato Nagahiro
発行年月	2011/02
概要	Programmed cell death-1 (PD-1) is an inhibitory receptor and plays an important role in the regulation of αβ T cells. Little is known, however, about the role of PD-1 in γδ T cells. In this study, we investigated the expression and function of PD-1 in human γδ T cells. Expression of PD-1 was rapidly induced in primary γδ T cells following antigenic stimulation, and the PD-1(+) γδ T cells produced IL-2. When PD-1(+) γδ T cells were stimulated with Daudi cells with and without programmed cell death ligand-1 (PD-L1) expression, the levels of IFN-γ production and cytotoxicity in response to PD-L1(+) Daudi cells were diminished compared to the levels seen in response to PD-L1(-) Daudi cells. The attenuated effector functions were reversed by anti-PD-L1 mAb. When PD-1(+) γδ T cells were challenged by PD-L1(+) tumors pretreated with zoledronate (Zol), which induced γδ TCR-mediated signaling, the resulting reduction in cytokine production was only slight to moderate compared to the reduction seen when PD-1(+) γδ T cells were challenged by PD-L1(-) tumors. In addition, cytotoxic activity of PD-1(+) γδ T cells against Zol-treated PD-L1(+) tumors was comparable to that against Zol-treated PD-L1(-) tumors. These results suggest that TCR triggering may partially overcome the inhibitory effect of PD-1 in γδ T cells.
DOI	10.1002/eji.201040959
PMID	21268005