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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
CD95 is cytoprotective for intestinal epithelial cells in colitis
Sun-Mi Park1, Lina Chen, Manling Zhang
1Ben May Department for Cancer Research, Johns Hopkins Medical Institute, Baltimore, Maryland, USA.
Inflammatory Bowel Diseases
|January 6, 2010
Summary
CD95 protects the colon from inflammation but does not impact colon cancer development. Mice lacking CD95 signaling in the colon showed increased sensitivity to colitis.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- CD95 (tumor necrosis factor receptor superfamily) is expressed on intestinal epithelial cells (IECs) and can induce apoptosis.
- The role of CD95/CD95L signaling in gut physiology, inflammation, and cancer is debated.
- Evidence for CD95 involvement in normal epithelial cell turnover is limited.
Purpose of the Study:
- To investigate the role of CD95 signaling in the colon during inflammation and cancer.
- To determine if CD95 deficiency in IECs affects colitis or colon cancer development.
Main Methods:
- Generated CD95 signaling-deficient mice via bone marrow transplantation or tissue-specific deletion in IECs.
- Induced colitis using dextran sulfate sodium (DSS) and colon cancer using azoxymethane (AOM)/DSS.
- Assessed disease index, lesion formation, and performed histological analysis.
Main Results:
- Mice lacking CD95 activity in the colon exhibited hypersensitivity to DSS-induced colitis.
- Colon cancer formation induced by AOM/DSS was not affected by CD95 deficiency in colon cells.
Conclusions:
- CD95 signaling is crucial for protecting the colon against inflammation.
- The CD95/CD95L system does not appear to contribute to colon cancer development in this model.
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