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Abstract. The antibodies encountered in random collectives of 55,350 recipients, 16,643 pregnant women, and 1,307 mothers of babies with hemolytic disease are listed. Antibody screening was performed in all specimens using the same technique (albumin‐antiglobulin test), a limited number of selected sera was investigated also by the auto‐analyzer. Different frequencies of the antibodies concerned were found in all groups. Anti‐Kell was detected in 10% of all antibodies found in recipients whereas the frequency was less than 0.5% among the antibodies encountered in pregnant women and mothers of babies with hemolytic disease. The relative antigenic potency of the antigens concerned was calculated by taking into account the frequencies of the antibodies and the antigen exposure probability derived from the well‐known gene frequencies. Similar to the antibody frequencies, the relative antigenic potencies differ widely from antigen to antigen in the different collectives. By the autoanalyzer technique, it was not possible to detect additional antibodies of presumptive clinical importance. On the other hand, in two exceptional cases, antibodies which caused a hemolytic transfusion reaction were only detected by survival studies. For routine transfusion work, our results lend no support to the alleged advantage of extending antigen determination in donors and recipients.

Islet cell antibodies (ICAs) were determined in a large cohort of white nondiabetic schoolchildren (n = 4287) from a homogenous population in southern Germany. The prevalence of ICA levels ≥5 Juvenile Diabetes Foundation (JDF) U was 1.05% (95% confidence interval 0.8–1.4%). Analysis of HLA-DRβ and -DQβ alleles revealed that the specificities found to be increased in insulin-dependent (type I) diabetic subjects with the same ethnic background were also associated with ICA positivity in the nondiabetic schoolchildren. HLA-DR3 (P < 0.01) and -DR4 (P < 0.01) phenotypes and absence of Asp residue (P < 0.01) at codon 57 of the HLA-DQ β-chain were significantly increased in ICA+ compared with control subjects. High levels of ICAs, which were categorized as either ≥17 or ≥30 JDF U, were found to be associated with amino acids other than Asp at position 57 of the HLA-DQ β-chain. No association of ICA level was found for HLA-DR phenotypes.

Graves' disease (GD) is a human leukocyte antigen (HLA) linked organ-specific autoimmune disease. In German GD patients the disease is associated with HLA specificities of the HLA-DRw52 family (HLA-DR3, -DR5, and DR6; HLA-DRB3 positive HLA haplotypes). Recently, a strong association with a HLA-DRB3 restriction fragment length polymorphism gene has been described. To study HLA-DRB3 alleles and their association with the disease, a large cohort of controls (n = 3724) and GD patients (n = 304) was analyzed. HLA-DR allelic combinations revealed an increase in HLA-DR3/DR5 heterozygous patients (relative risk 2.9; P < 0.001). HLA-DRB3 alleles, as defined by DNA typing in HLA-DR matched groups revealed a significant increase in DRB3*0101 homozygosity (relative risk 17.5; P < 0.001) in HLA-DR3 homozygous patients. In GD patients with ophthalmopathy (grade II or higher, according to Werner) DRB3*0101/*0202 heterozygosity revealed an increased relative risk of 5.5 (P < 0.001). Non-HLA-DR3 homozygous, DRB3*0101/*0202 heterozygous patients were at the highest risk for endocrine ophthalmopathy (relative risk 10; P < 0.001). Our data, based on DNA typing methods of HLA-D genes, provide evidence that the susceptibility is strongly associated with HLA-DRB3 genes.

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