Selective reduction of anti‐Helicobacter pylori IgG subclass antibody in gastric carcinoma

Abstract

Epidemiological studies have demonstrated strong links between Helicobacter pylori infection and gastric adenocarcinoma. Recent studies suggest that cell-mediated immunity influences the outcome of infection, including the development of gastric adenocarcinoma. The T-cell response can be characterized in terms of the secreted cytokine profile, which in turn influences the B-cell response including the balance of IgG subclass antibody. Serum anti-H. pylori IgG, IgG1 and IgG2 antibodies were studied by ELISA in subjects with benign gastric diseases, gastric dysplasia and gastric adenocarcinoma. The distribution patterns of IgG subclass anti-H. pylori antibody varies significantly between H. pylori-linked benign and malignant disease in subjects infected with H. pylori. Significantly lower IgG2 levels were found in subjects with gastric adenocarcinoma compared with those with reflux esophagitis, chronic gastritis, gastric ulcer, and peptic ulcer, while IgG1 antibody remained at similar levels in both benign and malignant disease. A limited study of seropositive subjects with premalignant change was consistent with the fall in IgG2 antibody pre-dating malignant change, although pre-eradication results are needed to validate these data. These studies indicate that subjects with low levels of IgG2 anti-H. pylori antibody are at risk of gastric adenocarcinoma, and that the previously described linkage between gastric adenocarcinoma and low total IgG antibody does not simply reflect reduced gastric colonization. The diagnostic value of this assay for pre-endoscopy screening is attractive.