ENHANCED HUMORAL IMMUNE RESPONSE TO TUMOR-ASSOCIATED T GLYCOTOPE (GALb1,3–GalNAc) IN HELICOBACTER PYLORI-INFECTED PATIENTS WITH GASTRIC CANCER AND NON-TUMOR GASTRIC DISEASES

Klaamas K., Kurtenkov O., Brjalin V., Miljukhina L., Shljapnikova L., Engstrand L.

Natural carbohydrate-binding antibodies are considered to play a role in host defence against infections and neoplasia. We aimed to study whether H.pylori infection influences natural immune response to tumor-related T glycotope. A level of T-specific antibodies in serum of H.pylori-infected and uninfected blood donors (n = 191), patients with gastric cancer (n = 186) and non-tumor gastric disorders (n = 126) was detected by ELISA using T-disaccharide-polyacrylamide conjugate as antigen. H.pylori status was evaluated with ELISA and Lewis (a, b) phenotyping of erythrocytes with monoclonal antibodies. The Se/se status was determined by testing of H-antigen in saliva. Expression of T epitope in H.pylori was evaluated by immunoblotting. An increased IgG response to T antigen was observed in all H.pylori-infected groups compared to uninfected controls. The differences were significant for patients with gastric cancer and gastritis (p < 0.05). The H.pylori-uninfected patients with peptic ulcer revealed the lowest level of IgG T-antibody. An increased IgG response in infected individuals was mostly related to the subjects of Le(b-) phenotype. А decrease of T antibody level was observed after H.pylori eradication in patients with high level of antibodies before treatment. In H.pylori extracts, two protein bands (58 kDa and 68 kDa) were immunostained with T epitope-specific monoclonal antibodies. In conclusion, the H.pylori infection is associated with an increased immune response to cancer-associated T epitope. This systemic impact appears to be dependent on Lewis phenotype of the host, in part disease type-specific and might be explained by T epitope expression in H.pylori. These findings suggest that H.pylori may be indirectly involved in gastric carcinogenesis via modulation of natural cancer-related immune mechanisms.

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