Table 2. Frequencies of HLA-DRB1 alleles Healthy controls (%) DRB1 n = 129 Type 2 DM (%) Non-diabetic ASO (–) n = 76 ASO (+) n = 28 ASO n = 17 0101 0301 0401 0403 0404 0405 0406 0407 0410 0802 0803 0804 0901 1001 1101 1201 1202 1301 1302 1401 1402 1403 1405 1406 1407 1501 1502 1601 1602 17.8 0.8 0.8 1.6 0.8 20.2 13.2 1.6 4.7 14.0 17.8 2.3 20.2 0.8 2.3 5.4 0 3.9 11.6 4.7 0.8 3.9 4.7 3.1 0.8 11.6 21.7 1.6 2.3 13.2 0 0 0 0 38.2 5.3 0 2.6 6.6 19.7 1.3 22.4 0 5.3 1.3 2.6 1.3 6.6 1.3 0 2.6 1.3 1.3 0 35.5a 19.7 1.3 3.9 DM: diabetes mellitus. ASO: arteriosclerosis obliterans. a P < 0.05 (χ2 = 4.187). b P < 0.01 (χ2 = 11.745). c P < 0.05 (χ2 = 5.642). 10.7 0 0 0 0 21.4 3.6 0 3.6 3.6 17.9 3.6 17.9 0 3.6 0 0 3.6 7.1 3.6 0 0 0 3.6 0 60.7b 17.9 3.6 3.6 11.8 0 0 0 0 23.5 5.9 0 5.9 5.9 23.5 0 17.6 0 5.9 0 0 0 11.8 5.9 0 0 0 0 0 52.9c 17.6 5.9 5.9 Figure 1. Relative frequencies of HLA-DRB1*1501 in type 2 diabetes and ASO patients. N.S. not signiﬁcant. Results Table 2 shows the HLA-DRB1 alleles in the control and type 2 diabetes patients. The incidence of HLA-DRB1*1501 © 2006 The Authors Journal compilation © 2006 Blackwell Publishing Ltd, International Journal of Immunogenetics 33, 117–122 HLA/NA/HPA in type 2 diabetes and ASO 119 Table 3. Results of genotyping of FcγRIIIB in healthy controls and patients Genotypes NA1/NA1 NA1/NA2 NA2/NA2 a P < 0.05 (χ2 = 4.570). b P < 0.05 (χ2 = 4.892). Healthy controls n = 129 48 (37.2%) 65 (50.4%) 16 (12.4%) Type 2 DM Non-diabetic ASO (–) n = 76 22 (28.9%) 36 (47.4%) 18 (23.7%) ASO (+) n = 28 3 (10.7%) 14 (50.0%) 11 (39.3%)a ASO n = 17 2 (11.7%) 8 (47.1%) 7 (41.2%)b was found to be signiﬁcant in type 2 diabetes and non- diabetic ASO-positive patients compared to controls (con- trol vs. ASO-negative diabetic patients, 11.6% vs. 35.5%, P < 0.05; control vs. ASO-positive diabetic patients, 11.6% vs. 60.7%, P < 0.01; control vs. non-diabetic ASO-positive patients, 11.6% vs. 52.9%, P < 0.05). In addition, the incidence of this allele was found to be signiﬁcant in ASO patients compared to non-ASO patients, although there was no signiﬁcant difference between diabetic and non- diabetic patients (Fig. 1). On the other hand, another DRB1 allele did not exhibit signiﬁcant differences. Table 3 shows gene frequency in control and type 2 diabetes patients; there were no differences in NA1/ NA2 among the control, type 2 diabetes and non-diabetic ASO groups. However, the frequency of NA2/NA2 in ASO-positive diabetic and non-diabetic ASO patients was signiﬁcantly higher than in controls (control vs. ASO- negative diabetic patients, 12.4% vs. 23.7%, N.S.; control vs. ASO-positive diabetic patients, 12.4% vs. 39.3%, P < 0.05; control vs. non-diabetic ASO-positive patients, 12.4% vs. 41.2%, P < 0.05). Table 4 shows the HPA genotypes of the control and diabetic patients. The a/b genotype of HPA-5a/5b was signiﬁcantly lower in type 2 diabetes and non-diabetic ASO patients than in controls (Control vs. ASO-negative diabetic patients, 7.0% vs. 1.3%, N.S.; control vs. ASO- positive diabetic patients, 7.0% vs. 0%, P < 0.05; control vs. non-diabetic ASO-positive patients, 7.0% vs. 0%, P < 0.05). Discussion Polymorphisms of class II genes within the major histo- compatibility complex can now be precisely determined by typing using the PCR–RFLP method. For example, serologically deﬁned HLA-DR antigens can be divided into many alleles reﬂecting the polymorphism of the amino acid sequence in the allelic hypervariable regions of the β chain. In addition, it has been reported that aplastic anemia patients with HLA-DR2 are likely to respond to immunosuppressive therapy (Nimer et al., 1994; Nakao et al., 1994). We have reported that the frequency of HLA-DR decreased and that of DRB1*0410 signiﬁcantly increased in immune thrombocytopenic purpura patients with poor response to prednisolone (Nomura et al.,