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  • Title: Expression of class I and II MHC receptors in Helicobacter pylori-positive patients with active gastritis and duodenal ulcer.
    Author: Suleymanov Z.
    Journal: Turk J Gastroenterol; 2003 Sep; 14(3):168-72. PubMed ID: 14655059.
    Abstract:
    BACKGROUND/AIMS: Helicobacter pylori colonizes on the epithelial surface below the mucous membrane in the gastric antrum, causing chronic active gastritis and duodenal ulcer. However, we know little about the response of the immune system, which is responsible for protecting the organism, to this bacteria and the duodenal tissue damage. The aims of our study were to examine the expression of class I and II MHC receptors in the immune cells in the peripheral venous blood of patients with chronic active gastritis and duodenal ulcer. METHODS: The study included a total of 124 cases (Helicobacter pylori-positive patients without prior treatment, 47 of whom had small-sized and 56 medium-sized duodenal ulcer, and 21 healthy individuals). Immune cells carrying receptors CD3, CD4, CD3/4, CD8, CD3/8, CD14, CD45, CD14/45, HLA-DR, CD3/HLA-DR, CD16/56, and CD3/16/56 by applying DAKO Dual Color Reagent, and non-specific indicators of reactivity, were investigated in the peripheral venous blood samples. RESULTS: In both study groups, nonspecific indicators of reactivity in peripheral venous blood were not different from those in the healthy group irrespective of the ulcer size. It was detected that NK cells which express only CD3/16/56 receptor are more aggressive than class I MHC carriers, which were increased in both patient groups more markedly than in the control group (p<0.05). The number of CD14 cells in patient groups with small- and medium-sized duodenal ulcers was found to be lower than in the control group. This difference was more marked in the small-sized ulcer group than in the medium-sized ulcer group. While there was a similarity in the number of CD45 cells in all three groups, the number of CD14/45 cells was reduced in the study group. This reduction was found statistically insignificant in the medium-sized ulcer group, but significant in the small-sized ulcer group (p<0.05). As compared to the control group, the number of HLA-DR cells was found to be increased in both study groups, and CD3/HLA-DR was found to be increased in the medium-sized ulcer group (p<0.05). CONCLUSIONS: The reduced number of CD14 cells may have been among the factors predisposing to the development of Helicobacter pylori infection. Such a deficit in cellular defense may be compensated through the upregulation of cells with HLA-DR and CD3/HLA-DR markers by the organism. The increase in the number of cells expressing CD3/16/56 in chronic antral gastritis and duodenal ulcer patients positive for Helicobacter pylori suggests a role for autoimmune events in these diseases.
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