| 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
|
| Resource |
| Mice |
RBRC04903 |
