To determine genetic susceptibility factors for Helicobacter pylori infection, polymorphic T-cell receptor gene elements were investigated in 203 H. pylori-infected individuals and 180 uninfected individuals (controls).H. pylori infection is highly associated with individuals homozygous for the nonfunctional TCRBV6S1B element (odds ratio ‫؍‬ 5.9; 2 ‫؍‬ 13; P ‫؍‬ 0.00032; P value corrected for multiple comparisons [Bonferroni correction] ‫؍‬ 0.00063).Presentation of bacterial antigens and recognition via T lymphocytes play a central role in the immune response to most bacterial antigens, including Helicobacter pylori (1, 6). We investigated three highly polymorphic microsatellites, TCRBV6S7, TCRBV6S1, and TCRBV6S3 (3, 7), and correlated them with exonic polymorphisms of the T-cell receptor (4) for associated susceptibility to H. pylori infection.A total of 383 unrelated, German individuals (ranging in age from 16 to 94 years; mean age, 59 years) undergoing gastroesophageal duodenoscopy for various clinical indications such as upper abdominal pain or noncardiac chest pain were included in this study after giving informed consent. Persons with a history of eradication therapy, acid-suppressive therapy within the last 4 weeks, evidence of malignancy, immunosuppression, or history of gastric surgery were excluded. H. pylori status was determined by rapid urease test, culture, and histology. At least two procedures had to yield positive results before subjects were considered infected. Individuals were considered H. pylori negative if all tests gave negative results. If one test result differed from the other two, serology was performed (Helicobacter pylori IgG ELISA kit; Medac, Hamburg, Germany). A total of 203 individuals were determined to be H. pylori positive and 180 individuals were determined to be H. pylori negative. In the H. pylori-positive group, 40 individuals suffered from gastric ulcer or had a history of gastric ulcer and 40 individuals had developed duodenal ulcer. There was no evidence for acute ulceration or history of ulcer disease in 123 individuals.DNA preparation and microsatellite analysis were performed as described previously (8,11). Haplotype frequencies were estimated by using ARLEQUIN software (standard deviation computed by 50 bootstraps) (14). Allele frequencies and estimated haplotype frequencies were compared by using a 2 ϫ 2 contingency table and 2 statistics and were considered significantly different if the P values were Ͻ0.05. Differences in allele or genotype distribution between the infected cohort and control cohort were quantitated using odds ratios (OR). Only

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