| First Author | Shapiro M | Year | 2017 |
| Journal | Oncoimmunology | Volume | 6 |
| Issue | 1 | Pages | e1261776 |
| PubMed ID | 28197386 | Mgi Jnum | J:350612 |
| Mgi Id | MGI:7664232 | Doi | 10.1080/2162402X.2016.1261776 |
| Citation | Shapiro M, et al. (2017) Deficiency of the immunostimulatory cytokine IL-21 promotes intestinal neoplasia via dysregulation of the Th1/Th17 axis. Oncoimmunology 6(1):e1261776 |
| abstractText | IL-21 has reported activity in promoting both Th1 and Th17 immune responses. Its role in sporadic human colorectal cancer is unknown. We aimed to delineate the role of IL-21 in a model of sporadic intestinal carcinogenesis. We found that in APC(MIN/+) mice, ablation of IL-21 increased intestinal tumorigenesis. Expression of pro-inflammatory Th17-associated genes, including RORgammat and IL-17A, was increased in the intestine in the absence of IL-21, while expression of antitumor Th1-associated genes Tbet, IFNgamma, granzyme B, and perforin was decreased. Similarly, the IL-21-deficient APC(MIN/+) mouse intestines had fewer infiltrating T cells as well as decreased effector memory T cells, NK cells, and granzyme B-expressing cells. Finally, our data suggest that IL-21 impairs Th17 immune responses as mesenteric lymph nodes from IL-21-deficient mice had increased IL-17A expression, and naive helper T cells from IL-21-deficient mice were more prone to differentiate into IL-17A-secreting cells. |
