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PubMed1984

Linkage disequilibrium between the HLA-B14 subdivisions and HLA-A, DR and properdin factor B alleles.

The recently reported linkage disequilibrium between HLA-B14.1 and DR7 and B14.2 and DR1 has been confirmed in a study of 44 B14.1 and 40 B14.2 positive individuals. In addition, significant linkage disequilibrium was observed between BfF and B14.2. Data on 238 B14 positives (98 B14.1 and 140 B14.2), from a population of 4,238, continues to support the previous observation of associations between B14.1 and Aw32 and B14.2 and A3, A28 and Aw33. These findings add further evidence for the existence of B14 splits.

Alleles↗
PubMed1980

High frequency of the properdin factor Bf F1 and its linkage to HLA in French Basques.

We studied 201 unrelated French Basque individuals for HLA and Bf polymorphisms. The haplotypes of eighty-seven of them were deduced from family studies. The results show the frequency of the Bf F1 allele (0.1393) which is the highest one currently reported. They confirm the high frequencies of HLA-Aw19.2 and B18 previously reported in that population and show that a whole haplotype with strong linkage disequilibria, namely Aw19.2, Cw5, B18, Bf F1, DRw3 is frequent. On the other hand, the gene frequency of Bf S is decreased (0.5497) as compared with the other European Caucasoïd populations, while a slight increase in the Bf F gene frequency (0.2960) appears. These results point out that it is of importance to consider the genetic background choosing the population where linkage disequilibria are to be studied.

Alleles↗
PubMed1979

Properdin factor D: effects on thrombin-induced platelet aggregation.

Factor D, when preincubated with platelet suspensions, at concentrations as low as 1.2 micrograms/ml, inhibited thrombin-induced platelet aggregation. No inhibition of collagen or arachidonic acid-induced platelet aggregation was found. Inhibition occurred, but to a lesser extent, when thrombin and factor D were added to platelets at the same time. No inhibition occurred when factor D was added after thrombin. Thrombin was able to overcome inhibition by factor D by increasing its concentration. Diisopropyl-phosphorofluoridate-inactivated factor D also inhibited thrombin-induced platelet aggregation so that enzymatic activity of factor D was not required for inhibition. Factor D absorbed with hirudin coupled to Sepharose 6B showed no decrease in inhibitory capacity. 125I-Factor D bound to platelets in a manner suggesting an equilibrium reaction similar to thrombin. At low factor D input, binding was linear, whereas at higher input, binding began to approach saturation. Binding of 125I-labeled thrombin to platelets was inhibited by factor D. Analysis of these data show that factor D does not alter the total number of thrombin molecules which bind to the platelet surface at saturation. However, the dissociation constant for thrombin is altered from 2.78 to 6.90 nM in the presence of factor D (20 micrograms/ml). Factor D is thus a competitive inhibitor of thrombin binding, although the affinity of factor D for the platelet thrombin receptor is much less than that of thrombin. These phenomena occur at physiologic concentrations of factor D. Therefore, factor D may function in vivo as an inhibitor of platelet aggregation.

Binding, Competitive↗
PubMedDate not supplied

Inhibition of human factor B activity of the properdin system by human and guinea-pig sera.

The activity of factor B of the alternative pathway of complement activation was assayed in human and guinea-pig sera using the radial haemolytic assay with various MgCl2 and RB concentrations. RB were prepared by heating at 50 degrees C human or guinea-pig sera to render them deficient in factor B. Whatever concentrated RB and MgCl2 were, guinea-pig sera seemed unable to react while human sera gave an haemolytic reaction with both human and guinea-pig RB. We described an inhibition of human factor B activity by human and guinea-pig RB under certain conditions. This inhibition is more pronounced in the case of guinea-pig RB.

Animals↗