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Human colonic intra-epithelial lymphocytes are suppressor cells
P Hoang1, H R Dalton, D P Jewell
1Gastroenterology Unit, Radcliffe Infirmary, Oxford, England, UK.
Clinical and Experimental Immunology
|September 1, 1991
Summary
Human colonic intra-epithelial lymphocytes (IEL) suppress specific immune cells but not others. This function, mediated by a soluble factor, is intact in inflammatory bowel disease, suggesting a role in mucosal tolerance.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- Human colonic intra-epithelial lymphocytes (IEL) play a role in mucosal immunity.
- Understanding IEL function is crucial for mucosal tolerance and inflammatory bowel disease (IBD).
Purpose of the Study:
- To investigate the suppressor function of human colonic IEL on autologous immune cells.
- To determine the mechanisms underlying IEL-mediated suppression and its relevance in IBD.
Main Methods:
- Human colonic IEL and autologous lamina propria lymphocytes (LPL) or peripheral blood mononuclear cells (PBMC) were isolated.
- Proliferation assays were performed using phytohaemagglutinin (PHA) stimulation.
- Flow cytometry and functional assays were used to characterize the suppressor mechanism.
Main Results:
- Colonic IEL suppressed autologous LPL proliferation but not autologous PBMC proliferation when stimulated with PHA.
- This suppressor function was mediated by a CD8-dependent soluble factor.
- Gamma delta T cell receptor expression was not related to the suppressor function.
- No defect in suppressor activity of colonic IEL was observed in patients with inflammatory bowel disease.
Conclusions:
- Human colonic IEL possess a specific suppressor function against autologous LPL, mediated by a CD8-dependent soluble factor.
- This suppressor activity is independent of gamma delta T cell receptor expression.
- The intact suppressor function of colonic IEL in IBD suggests it may not be directly involved in IBD pathogenesis but could be relevant for mucosal tolerance induction.