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PubMed1985

Another family with a silent allele of properdin factor B polymorphism (BF QO).

In five of eight members of a three generation family the existence of a silent allele of the properdin factor B polymorphism (BF QO) was indicated by immunofixation of BF electrophoretic variants and by the hemolytic overlay after isoelectric focusing of BF allotypes. This was further supported by the results of HLA-A, B, C, DR, C2, C4A, C4B, GLO-typing. BF protein was decreased in all heterozygous BF deficient family members. The absolute hemolytic activity, however, was obviously compensated for by an increased relative functional activity of the normal S or F alleles on the other chromosome.

Alleles↗
PubMed1983

Properdin factor B (Bf) polymorphism: subtyping of SS phenotypes.

The authors have studied the genetic polymorphism of the properdin factor B (Bf) by the isoelectrofocusing technique. The SS phenotypes, all similar on agarose gel electrophoresis, were shown to be heterogeneous after isoelectrofocusing; this heterogeneity corresponds to the expression of two new suballeles SA and SB, inherited in a codominant manner. Gene frequencies for 121 individuals with SS phenotype are 0.57 for SA, and 0.43 for SB.

Alleles↗
PubMed1979

Properdin factor B-polymorphism. An indication for the existence of a Bf O-allele.

The polymorphism of the properdin factor B (Bf, C3-proactivator, GBG = glycin-rich-beta-glycoprotein) has been investigated by high voltage agarose gel immunofixation electrophoresis in 1115 unrelated persons from Southern Germany. Seven phenotypes were observed; the allele frequencies were calculated as BfS = 0.8094, BfF = 0.1790, BfSI = 0.0094, BfFI = 0.0022. A study of 94 parents with 98 children and 420 mother-child combinations showed no deviation from the assumed autosomal codominant mode of inheritance. In one additional family the findings suggested the existence of a silent allele at the Bf-locus.

Alleles↗
PubMed1982

Associations of properdin factor B with melanoma.

We investigated 98 melanoma patients and 135 normal controls for differences in phenotype and genotype frequencies at the properdin factor B locus. A significant negative association with the Bf-F allele and melanoma was found, resulting in an estimated relative risk of 0.5. The estimated relative risk for developing melanoma among people with the Bf-FF genotype is 0.07. The Bf-S phenotype was significantly increased among the melanoma sample, with an estimated risk of 6.5. The data suggest association of the Bf locus with a melanoma protection and/or susceptibility gene(s).

Complement Factor B↗
PubMed1992

Properdin factor B and complement factor C4 allotypes in rheumatoid arthritis: results of a follow-up study.

The association between allotypes of properdin factor B (Bf), the fourth component of complement (C4A and C4B), and rheumatoid arthritis (RA), was investigated in a well-characterized cohort of RA patients who were followed from an early phase of the disease for a mean duration of 6 years. The frequencies of probable heterozygous C4AQ0 and of C4A3 were lower in RA patients compared to controls, irrespective of the presence of DR4 [relative risk (RR): 0.52 and 0.49, respectively, 95% confidence intervals (95% CI): 0.34-0.80 and 0.29-0.82]. The frequency of C4A4 was higher in RA patients compared to controls (RR: 1.86, 95% CI: 1.03-3.35), especially in DR4 positive RA patients compared to DR4 positive controls (RR: 2.58, 95% CI: 1.07-6.25), indicating a positive association of this allotype with RA additional to DR4. Bf and C4B allotypes were comparable in RA patients and controls. We did not find significant differences in Bf and C4 allotype frequencies in RA patients subdivided according to severity of the disease into a mild group and a progressive group. Because of inconsistent results in all studies on Bf and C4 allotypes, we conclude that C4 and Bf allotypes do not seem to have an important independent effect on determining disease susceptibility.

Adult↗
PubMed1981

Allotypic variants of human C3 and properdin factor B in two French populations Normans and Basques.

Human Properdin factor B and C3 polymorphisms are of a real usefulness as genetic markers for population studies. In addition, they are more and more used for the determination of paternity cases. The present communication will be about Bf and C3 allele frequencies in two locally populations of France, Normandy and Western Pyrenees (Basques), The corresponding allele frequencies are as follows, for Normans : Bf(S) = 0.7422, Bf(F) = 0.2285, Bf(F1) = 0.0205, Bf(SO.7) = 0.0088; CsS = 0.788, C3F = 0.204, C3Srare = 0.004, C3Frare =0.004; and for Basques : BfS = 0.5625, BfF = 0.305, BfF1 = 0.1235, BfSO.7 = 0.0075; C3S = 0.7075 and C3F - 0.2925. French Basques are characterized by unusual allele frequencies in European Caucasoid populations for Bf as for C3 genes. A very high incidence of BfF1 allele is reported (BfF1 = 0.125), as previously observed [7, 17].

Alleles↗
PubMed1984

Association between rapidly progressive glomerulonephritis and the properdin factor BfF and different HLA-D region products.

Frequencies of the HLA antigens ABC, DR and MT, as well as of the properdin factor alleles were determined in 24 unrelated patients presenting with immune complex mediated idiopathic rapidly progressive glomerulonephritis (RPGN) type II. As in Goodpasture syndrome (RPGN type I with pulmonary hemorrhage), a significant association with the B-cell alloantigen HLA-DR 2 was demonstrated (relative risk for HLA-DR 2 positive individuals was 3.54; P less than 0.01). In addition a marked increase of the HLA specificity MT 3 was shown, which is supposed to belong to an antigen system of a second HLA-D region locus. The highest relative risk of 14.67 (P less than 0.00001), however, was calculated for all patients carrying the BfF phenotype. Increased numbers of patients positive for HLA-DR 2 and -MT 3, as well as BfF suggested immune response genes or disease-related mutations on different haplotypes responsible for a MHC (major histocompatibility complex) associated predisposition of RPGN type II.

Adolescent↗
PubMed1998

Genetic polymorphism of properdin factor B (BF) in domestic rabbit.

Genetic polymorphism of plasma properdin factor B (BF) was detected in domestic rabbit, Oryctolagus cuniculus, by means of isoelectric focusing and immunoblotting. The analysis of 298 individuals, corresponding to one French and two Portuguese populations, revealed the existence of six alleles, of which BF*A, B and C were common alleles, and D, F and G were rare ones.

Alleles↗
PubMed1974

Properdin factor D: characterization of its active site and isolation of the precursor form.

The activity of properdin factor D was measured by the generation of the hemolytically active cellular intermediate, EAC43B(D), bearing the C3b-dependent alternate pathway C3 convertase. Treatment of factor D with DFP prevented formation of EAC43B(D); thus, a serine esterase is essential for the generation of the alternate pathway C3 convertase, a situation analogous to the role of C1 in the formation of the classical C3 convertase, C42. The definition of factor D as a serine esterase prompted a search for its proenzyme form, and resulted in the chromatographic isolation from plasma of a single peak of trypsin-inducible factor D activity, distinct from activated factor D. Analytical gel filtration indicated an apparent mol wt of 25,000. This protein from which trypsin elaborated factor D activity, as assessed by the formation of EAC43B(D), the generation of the CoVF-dependent C3 convertase, and the cleavage of factor B in the presence of C3b, was designated "precursor factor D." The DFP resistance of precursor factor D, and the susceptibility of its trypsin-activated form to inactivation by DFP is analogous to the behavior of other plasma serine esterases, including C1.

Animals↗
PubMed1979

The induction of macrophage spreading by factor B of the properdin system.

Unstimulated mouse peritoneal macrophages attached to a glass substratum responded to activated human factor B (Bb) of the properdin system but not to native factor B with rapid spreading and a concomitant increase in their apparent surface area. Excellent correlation of the distribution of Bb protein and cell-spreading activity was found upon purification of Bb by ion-exchange and molecular seive chromatography and alkaline polyacrylamide gel electrophoresis. 1.6 microgram of purified Bb was sufficient to induce spreading in 50% of 5 x 10(4) glass attached macrophages within 1-2 h at 37 degrees C. Treatment of Bb with di-isopropyl-fluorophosphate indicated that the intact catalytic site of the serine-proteinase Bb was required for the initiation of macrophage spreading. The involvement of factor B in the induction of rapid cell spreading could also be indirectly demonstrated in an autologous system in which F(ab')2 fragments of an antiserum to mouse B prevented mouse macrophages from spreading in response to complement-activated mouse serum. These experiments suggest a role for factor B and the alternative pathway of complement fixation in the localization of mononuclear phagocytes to areas of inflammation.

Animals↗
PubMed1981

Matching for properdin factor B (Bf) in renal transplantation.

Forty-five donor and recipient primary cadaveric kidney transplant pairs were phenotyped for the properdin factor B (Bf) polymorphism. Graft survival was analyzed on the basis of Bf matching between donor and recipient. Patients receiving a Bf-identical kidney had significantly better graft survival than those receiving a Bf-incompatible kidney (P = 0.045). It is postulated that Bf, which maps in the major histocompatibility system, is a marker for genes of importance in kidney transplant survival.

Complement Factor B↗
PubMed1992

Genetic polymorphisms in the fourth component of complement (C4) and in properdin factor B (BF) in Japanese patients with palmoplantar pustulosis.

Genetic polymorphisms in the fourth component of complement (C4) and in properdin factor B (BF) were investigated in 49 and 32 Japanese patients with palmoplantar pustulosis (PPP), respectively. C4B2 was significantly increased in frequency, whereas no significant deviations were detected in BF compared with the controls. These results may indicate that complement polymorphisms are involved in the pathogenesis of PPP.

Adult↗
PubMed1981

HLA antigens associated with properdin factor B allotype BfF1.

Linkage disequilibrium has been described between HLA-B antigens and allotypes of properdin factor B (Bf). The association between HLA-B and DR antigens and the rate allotype BfF1 was investigated. In 27 HLA-A, B and DR typed individuals only one person was found who was DR3 negative but five who were B18 negative. Family studies showed that in nine cases B18, BfF1 and DR3 segregated as a haplotype; in another family which was B18 negative, BfF1 and DR3 segregated together. It is inferred that the Bf locus is more strongly associated with HLA-DR than with HLA-B.

Complement Factor B↗
PubMed1981

Properdin factor B polymorphism in Black Americans.

Properdin factor B is a genetically-controlled polymorphism that can be demonstrated by agarose gel electrophoresis. The Bf gene frequencies were determined for 194 blacks from the south-eastern United States. The frequencies for Bf-F, Bf-S, Bf-F1, and Bf-S1 are 0.626, 0.034, and 0.013, respectively. The south-eastern blacks have similar Bf frequencies to the South African blacks; however, both these groups are different from blacks from Boston. The frequency differences between south-eastern blacks and Boston blacks may be due to racial admixture differences found in the two populations.

Black People↗
PubMed1980

Properdin factor B polymorphism in Afghanistan.

The distribution of properdin factor B (Bf) phenotypes and gene frequencies was studied in four populations of Afghanistan: Hazaras, Pushtoons, Tajiks and Usbeks. Significant differences between Usbeks and the other three ethnic groups were observed. The distribution of gene frequencies in Usbeks was similar to that of European populations.

Afghanistan↗
PubMed1980

Properdin factor B (Bf) as an exclusion determinate in parentage testing.

Properdin factor B (Bf) was phenotyped on 519 paternity cases. Gene frequencies of BfF = 0.1870, BfF1 = 0.0105, BfS = 0.7985 and BfSO.7 = 0.0040 were observed in Minnesota Whites. Based on these values the exclusion probability is (p) = 0.1442. Bf accounted for 15% of the 88 observed exclusions. A technique is described for simultaneous electrophoresis of Bf and Gc on the same gel.

Complement Factor B↗
PubMed1981

Properdin factor B polymorphism in Portugal.

The distribution of properdin factor B (Bf) phenotypes and the corresponding gene frequencies in a population sample from Portugal was investigated by agarose-gel electrophoresis and immunofixation. The following gene frequencies were found in Portugal: BfS = 0.6535, BfF = 0.2775, BfS0.7 = 0.0263, and BfF1 = 0.0427.

Alleles↗
PubMed1982

Subtyping of properdin factor B (Bf) by isoelectrofocusing.

Properdin factor B (Bf) is a polymorphic protein in the human plasma. Two common alleles, BfS, BfF, and two rare alleles, BfF1, BfS1, have been demonstrated in Caucasians. We now report that BfF can be subtyped into two alleles, BfFa and BfFb by isoelectrofocusing. Family studies indicate that they are inherited in a co-dominant pattern. Gene frequencies for Caucasians are: BfS 0.808, BfF1 0.019, BfS1 0.005, BfFa 0.038 and BfFb 0.128.

Australia↗