The present study was proposed to investigate the role of Human Leucocyte Antigen HLA-class I (A and B) and class II (DR) antigens and blood group phenotypes in the aetiology of chronic atrophic gastritis in a sample of Iraqi patients. The patients were also evaluated for total and absolute counts of leucocytes, immunophenotypes of lymphocytes (CD3+, CD4+, CD8+ and CD19+ cells) and positivity of their sera for anti-Helicobacter pylori IgG antibody. Forty-nine patients with the disease were investigated during the periods January-October, 2006. The disease was clinically diagnosed by the consultant medical staff at Al-Kadhmiyah Teaching hospital in the Gastrointestinal Tract (GIT) and Liver Diseases Center. The diagnosis was based on clinical evaluation using endoscopy and a histopathological examination of the stomach mucosal biopsy. According to the point view of consultants, the patients were clinically subdivided into two groups according to the location of inflammation; corpus gastritis (31 patients) and antrum gastritis (18 patients). A control sample of 50 individuals (apparently healthy), matched for age, sex and ethnic background (Arab Muslims), were investigated. The patients were also further divided into Helicobacter pylori-positive (HP+) and H. pylori-negative (HP-) according to the presence of IgG anti-H. pylori antibodies in their sera. There were 32 patients (65.3%) positive for IgG anti-H. pylori antibodies, while 17 patients (34.7%) were sero-negative for IgG anti-H. pylori antibodies. At HLA-class I and class II regions, six antigens showed increased frequencies in the total patients or their subgroups as compared to controls. They were A3, A9, B17, DR2, DR3 and DR10. The A3 antigen showed a significant increase in the total patients and antrum gastritis patients, while DR10 was consistently increased in the patients, and the Relative Risk (RR) value showed a range from 8.21 in H. pylori-positive gastritis to 22.38 in H. pylori-negative gastritis, and the Etiological Fraction (EF) value also showed variations (total gastritis: 0.39; corpus gastritis: 0.41; antrum gastritis: 0.34; H. pylori-positive gastritis: 0.30; H. pylori-negative gastritis: 0.56). In contrast, the antigen A19 was consistently decreased in the patients with a Preventive Fraction (PF) value more than 0.30 (total gastritis: 0.38; antrum gastritis: 0.33; H. pylori-positive gastritis: 0.38; H. pylorinegative gastritis: 0.39). Also, this antigen was not recorded in corpus gastritis patients, moreover, this group of patients showed a further two positive associations, which were A9 and DR2, and the EF values of such associations were 0.42 and 0.38, respectively. The immunogenetic predisposition to develop chronic atrophic gastritis was further explored with other immunogenetic markers; they were ABO blood group phenotypes. Two phenotypes were important in this regard; A and O. The blood group A was significantly increased in total patients (46.7 vs. 18.0%) and almost their subgroups, while a reverse outcome was observed for blood group O (22.2 vs. 48.0%) as compared to controls. Such two observations may suggest that the first blood group is involved in the aetiopathogenesis of chronic atrophic gastritis, while the second confers some resistance to develop the disease. Investigating the CD profiles of peripheral lymphocytes revealed a significant decrease of CD3+ (55.3 vs. 79.4%) and CD4+ (25.7 vs. 39.5%) cells in total patients of chronic atrophic gastritis and their subgroups, while CD8+ lymphocytes did not show such variation. The CD4/CD8 ratio was also significantly decreased in patients (1.23 vs. 1.81%). In contrast CD19+ lymphocytes showed a significant increase in total patients (27.4 vs. 18.7%) and their subgroups. Such observations suggest the importance of these cells in the aetipathogenesis of the disease. Finally, the total and absolute counts of leucocytes showed no significant differences between patients (total and subtypes) and controls.