Epithelial Expression of MHC Class II Is Associated with Intraepithelial Lymphocytosis in Helicobacter pylori Gastritis
M Joo, SH Chang, HS Kim, KM Kim. Ilsan Paik Hospital, Inje Univerisity, Goyang, Gyeonggi, Republic of Korea; Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea
Background: Intraepithelial lymphocytosis in the stomach can occur in association with a variety of conditions, including Helicobacter pylori (H. pylori) infection, celiac sprue and crohn's disease. H. pylori is believed to be causally related to the development of lymphocytic gastritis (LG) characterized by a marked increase in the number of intraepithelial lymphocytes (IELs). However, it remains unknown how H. pylori infection contributes to increase gastric IELs. In the gastric mucosa with H. pylori infection, MHC class II or monocyte chemoattractant protein-1 (MCP-1) can be aberrantly expressed in the gastric epithelium, which modulates T cell response. The aims of this study were to evaluate the changes of gastric IELs in response to H. pylori infection and to investigate the role of expression of MHC class II or MCP-1 in the gastric intraepithelial lymphocytosis.
Design: The clinical and pathological findings, the number of IELs (on CD3, CD8, CD4, T cell restricted intracellular antigen-1 (TIA-1), and granzyme B (GrB) immunostainings), and expressions of MHC class II and MCP-1 were evaluated in 34 normal gastric mucosa (control group), 49 H. pylori gastritis (HPG) and 37 LG with H. pylori infection.
Results: Gastric IELs in association to H. pylori infection consisted of mixed populations of latent cytotoxic T cells (CTLs) (CD8+/TIA-1+/GrB-), activated CTLs (CD8+/TIA-1+/GrB+) and CD4+ T cells. Compared to normal controls, HPGs showed a significantly higher number of CD3+, CD8+, CD4+ or GrB+ IELs. Epithelial MHC class II expression showed significant differences between groups, whereas a significant difference in MHC class II expression in lamina propria or MCP-1 expression (either in epithelium or in lamina propria) was found between normal controls and HPGs, but not between HPGs and LGs. On univariate analysis, the IEL counts correlated with patient's age, H. pylori infection, mononuclear cell infiltration, and expressions of MHC class II and MCP-1. Multiple regression analysis demonstrated that epithelial expression of MHC class II was the most important factor associated with an increase of the IELs.
Conclusions: Expression of MHC class II or MCP-1 is associated with gastric intraepithelial lymphocytosis in patients with H. pylori infection, and epithelial expression of MHC class II may play an important role in the increase of gastric IELs.
Monday, March 22, 2010 1:00 PM
Poster Session II # 76, Monday Afternoon