Reference - Detail
| RRC ID | 88503 |
|---|---|
| Author | Nakamura-Shinya Y, Iguchi-Manaka A, Murata R, Sato K, Vo AV, Kanemaru K, Shibuya A, Shibuya K. |
| Title | DNAM-1 promotes inflammation-driven tumor development via enhancing IFN-γ production. |
| Journal | Int Immunol |
| 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. |
| Volume | 34(3) |
| Pages | 149-157 |
| Published | 2022-2-23 |
| DOI | 10.1093/intimm/dxab099 |
| PII | 6406999 |
| PMID | 34672321 |
| MeSH | Animals Antigens, Differentiation, T-Lymphocyte* / metabolism Inflammation / metabolism Interferon-gamma / metabolism Killer Cells, Natural Ligands Mice Neoplasms* T Lineage-Specific Activation Antigen 1 |
| IF | 3.519 |
| Altmetric score |
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| The most frequently cited source | X(Twitter) |
| Total number of mentions | 1 |
| Altmetric score changes over past 6months | 0.0 |
| Resource | |
| Mice | RBRC04903 |