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Th9 and Th17 Cells in Human Ulcerative Colitis-Associated Dysplastic Lesions
Guanglin Cui1,2, Aping Yuan1, Sveinung W Sørbye3
1Research Group of Gastrointestinal Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Clinical Medicine Insights. Oncology
|December 9, 2024
Summary
T helper 9 (Th9) and T helper 17 (Th17) cells accumulate in colitis-associated dysplasia (CAD) tissues. Their increased presence suggests a role in the transition from precancerous dysplasia to colitis-associated colorectal cancer (CAC).
Area of Science:
- Gastroenterology
- Immunology
- Oncology
Background:
- Inflammation drives colitis-associated colorectal cancer (CAC) development via a specific sequence.
- T helper (Th) subsets Th9 and Th17 cells are implicated in ulcerative colitis (UC) inflammation.
- Th9 and Th17 cells may promote colitis-associated dysplasia (CAD).
Purpose of the Study:
- To evaluate the presence and density of T lymphocytes, Th9, and Th17 cells in human UC and CAD tissues.
- To understand the role of Th9 and Th17 cells in the progression of UC to CAD and potentially CAC.
Main Methods:
- Immunohistochemistry (IHC) was used to analyze tissue samples.
- Quantified densities of CD3-positive T lymphocytes, P.U.1-positive Th9 cells, and IL-17A-positive Th17 cells.
- Compared cell densities across normal, UC, and CAD tissues, including dysplasia subgroups.
Main Results:
- T lymphocyte, Th9, and Th17 cell numbers generally increased from normal to UC to CAD tissues.
- These cells were prominent in the lamina propria and sometimes in the epithelium of CAD tissues.
- Th9 and Th17 cell densities were higher in CAD tissues compared to UC and control tissues, with slight differences between non-adenoma-like and adenoma-like dysplasia.
Conclusions:
- Accumulated Th9 and Th17 cells are part of the immune cellular makeup in CAD tissues.
- These cells may signify early changes facilitating the transition from dysplasia to CAC.
- Further research into Th9 and Th17 cell roles in CAC development is warranted.

