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In a series of 42 families with 101 children the linkage between HL-A and PGM3 could be confirmed (most likely recombination fraction for male equals 0.15).

The frequencies of 36 HL-A antigens of the SD-1, SD-2 and SD-3 locus have been determined in 20 patients with idiopathic Addison's disease and compared with those of 450 controls. No significantly different HL-A antigen frequencies could be observed in both groups. These findings are in contradiction to data reported by a Copenhagen group. Possible mechanisms which might have led to this discrepancy are discussed.

Using a theoretical model formulas for the calculation of the chance of paternity exclusion for 2 closely linked autosomal loci with multiple allelism between which linkage disequilibrium exists are presented. With some examples their practicability for the HL-A system is shown.

In 17 cases positive cytotoxic anti-HL-A antibodies were gained from 26 immunizated pairs. On the whole this corresponds to the data to be found in literature [10, 17]. The antibodies against the antigens of the I. locus will appear more rapidly, younger persons will form antibodies more easily. The difference in one single antigen results in favourable findings when the pairs are composed; in spite of that, however, cross-reacting antibodies may frequently be obtained, particularly when boostered to produce sera with a high titre. No side effects were detected in the immunizated group; yet there is a certain reason to suppose that the production of anti-HL-A sera by artificial immunization cannot be compared with the usual production of AB0 sera. The immunopathological significance of the HL-A-system is still elucidated insufficiently; by no means it is confined to histocompatibility. Only those institutes should be concerned with artificial immunization which are able to perform the necessary immunological controls exactly in each case.

2 patients with 13- and C9-rings are reported. On reviewing the phenotypical features of the published ring carriers and comparing them with our results we do not find any characteristic similarities. This can be explained by cytogenetical and biological findings. We are therefore inclined to reject the existence of clear-cut ring chromosome syndromes.

HL-A antigens were determined in 18 unrelated patients with Gilbert's syndrome and 3 families where this condition occurred in 2 generations. The data obtained do not point out an association between HL-A antigens and Gilbert's syndrome.

Using the data obtained by typing 450 unrelated people of the Viennese population, the phenotype and gene frequencies of 37 HL-A factors governed by the 3 SD loci were determined. The haplotype frequencies involving SD-1 und SD-2 genes were calculated and the associations between the 3 SD loci have been analysed.