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Published on: October 6, 2014
IL-17F deficiency inhibits small intestinal tumorigenesis in ApcMin/+ mice
Wook-Jin Chae1, Alfred L M Bothwell
1Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Abstract:
IL-17 plays an important role in gut homeostasis. However, the role of IL-17F in intestinal tumorigenesis has not been addressed. Here we demonstrate that ablation of IL-17F significantly inhibits spontaneous intestinal tumorigenesis in the small intestine of Apc(Min/+) mice. IL-17F ablation decreased IL-1β and Cox-2 expression as well as IL-17 receptor C (IL-17RC) expression, which were increased in tumors from Apc(Min/+) mice. Lack of IL-17F did not reverse the splenomegaly but partially restored thymic atrophy, suggesting a local effect of IL-17F in the intestine. IL-17F deficient Apc(Min/+) mice showed a significant decrease in immune cell infiltration in the lamina propria. Interestingly, the expression of IL-17A from CD4 T cells in the lamina propria remains unchanged in the absence of IL-17F. Collectively, our results suggest the proinflammatory and essential role of IL-17F to develop spontaneous intestinal tumorigenesis in Apc(Min/+) mice in the presence of IL-17A.
Insights
Interleukin-17F (IL-17F) promotes intestinal tumor development. Removing IL-17F significantly reduced spontaneous intestinal tumors in mice, highlighting its role in gut tumorigenesis.
Area of Science:
- Immunology
- Gastroenterology
- Oncology
Background:
- Interleukin-17 (IL-17) is crucial for gut homeostasis.
- The specific role of IL-17F in intestinal tumorigenesis remains unclear.
Purpose of the Study:
- To investigate the function of IL-17F in spontaneous intestinal tumorigenesis.
- To elucidate the molecular mechanisms underlying IL-17F's involvement in tumor development.
Main Methods:
- Utilized Apc(Min/+) mice lacking IL-17F to study spontaneous intestinal tumor formation.
- Analyzed gene expression (IL-1β, Cox-2, IL-17RC) and immune cell infiltration in tumor tissues and the lamina propria.
- Assessed systemic effects by monitoring splenomegaly and thymic atrophy.
Main Results:
- Ablation of IL-17F significantly inhibited spontaneous intestinal tumorigenesis in Apc(Min/+) mice.
- IL-17F deficiency led to decreased expression of IL-1β, Cox-2, and IL-17RC in tumors.
- Reduced immune cell infiltration in the lamina propria was observed in IL-17F deficient mice, suggesting a local effect.
- IL-17A expression from CD4 T cells remained unchanged, indicating IL-17F's distinct role.
Conclusions:
- IL-17F plays a critical, pro-inflammatory role in the development of spontaneous intestinal tumors in Apc(Min/+) mice.
- The findings suggest IL-17F is essential for intestinal tumorigenesis, acting locally and in conjunction with IL-17A.
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