Joan O’Keeffe and Anthony P. Moran should be considered as joint senior authors.
Natural Killer Cell Receptor+ T-Lymphocytes in Normal and Helicobacter pylori-Infected Human Gastric Mucosa
Version of Record online: 11 NOV 2008
© 2008 The Authors. Journal compilation © 2008 Blackwell Publishing Ltd
Volume 13, Issue 6, pages 500–505, December 2008
How to Cite
O’Keeffe, J., Gately, C. M., O'Donoghue, Y., Zulquernain, S. A., Stevens, F. M. and Moran, A. P. (2008), Natural Killer Cell Receptor+ T-Lymphocytes in Normal and Helicobacter pylori-Infected Human Gastric Mucosa. Helicobacter, 13: 500–505. doi: 10.1111/j.1523-5378.2008.00641.x
- Issue online: 11 NOV 2008
- Version of Record online: 11 NOV 2008
- Helicobacter pylori;
- gastric mucosa;
- natural killer receptor+ T-cells;
- natural killer T-cells
Background: Helicobacter pylori infection is associated with development of chronic inflammation and infiltration of immune cells into the gastric mucosa. As unconventional T-lymphocytes expressing natural killer cell receptors are considered to play central roles in the immune response against infection, a study investigating their frequencies in normal and H. pylori-infected gastric mucosa was undertaken.
Materials and Methods: Flow cytometry was used to quantify T-cells expressing the natural killer cell markers CD161, CD56, and CD94 in freshly isolated lymphocytes from the epithelial and lamina propria layers of gastric mucosa. Thirteen H. pylori-positive and 24 H. pylori-negative individuals were studied.
Results: CD94+ T-cells were the most abundant (up to 40%) natural killer receptor-positive T-cell population in epithelial and lamina propria layers of H. pylori-negative gastric mucosa. CD161+ T-cells accounted for about one-third of all T-cells in both compartments, but the lowest proportion were of CD56+ T-cells. Compared with H. pylori-negative mucosa, in H. pylori-infected mucosa the numbers of CD161+ T-cells were significantly greater (p = .04) in the epithelium, whereas the numbers of CD56+ T-cells were lower (p = .01) in the lamina propria. A minor population (< 2%) of T-cells in both mucosal layers of H. pylori-negative subjects were natural killer T-cells, and whose proportions were not significantly different (p > .05) to those in H. pylori-infected individuals.
Conclusions: The predominance, heterogeneity, and distribution of natural killer cell receptor-positive T-cells at different locations within the gastric mucosa reflects a potential functional role during H. pylori infection and warrants further investigation.