DNAM-1 promotes inflammation-driven tumor development via enhancing IFN-γ production. (21st October 2021)

• Record Type: Journal Article
• Authors: Nakamura-Shinya, Yuho; Iguchi-Manaka, Akiko; Murata, Rikito; Sato, Kazuki; Vo, Anh Van; Kanemaru, Kazumasa; Shibuya, Akira; Shibuya, Kazuko
• Is Part Of: International immunology. Volume 34:Number 3(2022)
• Page Start: 149
• Page End: 157
• Publication Date: 2021-10-21
• Subjects: CD4+ T cells -- tumorigenesis; Immunology -- Periodicals; 616.079
• DOI: 10.1093/intimm/dxab099
• Languages: English
• ISSNs: 0953-8178

Abstract

Abstract: DNAM-1 is an activating immunoreceptor on T cells and natural killer (NK) cells. Expression levels of its ligands, CD155 and CD112, are up-regulated on tumor cells. The interaction of DNAM-1 on CD8 + T cells and NK cells with the ligands on tumor cells plays an important role in tumor immunity. We previously reported that mice deficient in DNAM-1 showed accelerated growth of tumors induced by the chemical carcinogen 7, 12-dimethylbenz[a]anthracene (DMBA). Contrary to those results, we show here that tumor development induced by 12- O -tetradecanoylphorbol-13-acetate (TPA) together with DMBA was suppressed in DNAM-1–deficient mice. In this model, DNAM-1 enhanced IFN-γ secretion from conventional CD4 + T cells to promote inflammation-related tumor development. These findings suggest that, under inflammatory conditions, DNAM-1 contributes to tumor development via conventional CD4 + T cells. Abstract : DNAM-1-induced IFN-γ from CD4 + T cells can promote tumorigenesis Graphical Abstract: