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The distribution of properdin factor B (Bf) phenotypes and the gene frequencies were investigated in 918 Saudi Arabs. A high frequency of the 'rare' allele BFS0.7 was observed BfS0.7 = 0.1514). The frequencies of the common Bf alleles (BfS = 0.5174, BfF = 0.3213) are outside the corresponding ranges of BfS, BfF gene frequencies found in European Caucasoids.
The phenotype frequencies of properdin factor B (Bf) were studied in patients with (n = 47) and without (n = 66) a family history of schizophrenia and in controls. In patients with a family history of schizophrenia, a significant decrease of the FS type was found. No significant difference was found between patients without a family history of schizophrenia and controls.
The distribution of Properdin factor B (Bf) phenotypes and their gene frequencies were investigated in four Asian populations (Chinese, Filipino, Thai and Japanese). The frequency of the BfS phenotype in Filipinos (0.717) was significantly lower than that in Chinese (0.900) and Thai (0.889) (p less than 0.01), but not different from the Japanese (0.840). One variant, BfF 0.65 S, was identified in a Japanese subject. Thus, in the Asian populations studied, Bfs frequencies were high and the frequency of variants other than F and S were low.
A sample of healthy unrelated individuals was typed for properdin factor B (Bf) polymorphism in four Sardinian villages. Two villages, Desulo and Tonara, are located in the highlands; the other two, Orosei and Galtellì, are located in the lowlands. No heterogeneity was found between the highland and the lowland villages, whereas a significant difference was found between the Sardinian villages and continental Italy. The allele Bf-F1 shows the highest gene frequency so far observed. Typically Sardinian is the gametic association (haplotype) HLA-A30, Cw5, B18, BfF1, DR3.
We have investigated the properdin factor B(Bf) polymorphism in relation to lymphocytotoxic antibody production. The Bf phenotypes of 1,113 individuals was determined; these consisted of 360 cytotoxic antibody-negative normal healthy controls, 293 HLA typing antisera, 330 sera from pregnant multiparous women, and 130 renal patients awaiting cadaveric transplantation. The allotype BfF was found to be strongly associated with cytotoxic antibody production in multiparous women.
The serum levels of Ceruloplasmin (CER), Properdin Factor B (PFB) and Copper (CU) were evaluated in a series of 40 patients with Hodgkin's Disease and 46 patients with non-Hodgkin's lymphoma. Concentrations of CER and PFB were determined by rate nephelometry and CU concentrations by the bathocuproine colorimetric method. The results obtained demonstrated that CER, together with the well documented CU, can be used for monitoring Hodgkin's Disease.
The distribution of phenotypes controlled by two loci on chromosome 6 has been studied in a series of 239 patients with type 1 (insulin-dependent) and 297 patients with type 2 (non-insulin-dependent) diabetes mellitus. At the properdin factor B (Bf) locus there is a significant increase in the frequency of the BfSu and BfF1 alleles for type 1 patients, and the combined inc;rease in frequency of BfS1 and BfF1 in those patients is highly significant. The relative risk for F1 is 6.2 and for F1 and S1 combined is 5.3. These results confirm the association with F1 reported recently by Raum and co-workers in Boston. The two rare alleles BfS1 and BfF1 are in significant negative disequilibrium with HLA B8. For the glyoxalase (GLO) locus there is a slight but nonsignificant increase in the frequency of the GLO2 allele, but a significant disturbance in the distribution of the GLO phenotypes for type 2 patients. These results for the GLO alleles may be due to stratification in our series of type 2 patients. Further studies are in progress to test this hypothesis.
We found the rare properdin factor B(Bf) variant F1 to be present in 11% of 72 patients suffering from insulin-dependent diabetes (IDDM) compared with 2% among 150 normal controls. BfF1 thus confers a relative risk for IDDM of 5.55. All eight patients and three controls who were BfF1 positive were also HLA-B18 positive, reflecting the strong linkage disequilibrium between these two factors. We suggest that BfF1 marks a 'diabetogenic' B18-bearing HLA haplotype. Studies of unselected families with one or more affected members suggest that the B18, BfF1 does not necessarily segregate with IDDM phenotype. This study provides further evidence for the genetic heterogeneity of IDDM.
This study examines the distribution of properdin factor B by means of electrophoresis on cellulose acetate in a sample of 780 individuals from seven historical/geographical areas of Sardinia: Nurra, Goceano, Nuorese, Arborea, Sarcidano, Ogliastra, Campidano di Cagliari. The gene frequencies obtained for the total sample are BF*S = 0.595, BF*F = 0.227, BF*S1 = 0.012, BF*F1 = 0.166. Division of the total sample into subsamples has highlighted some noticeable differences both among the historical/geographical areas considered and with mainland Italy. In Sardinia relatively low frequencies of the allele BF*S are accompanied by exceptionally high incidences of the variant allele BF*F1, which reaches a maximum in the Goceano area (0.2143).
Properdin factor B(Bf) allotypes were determined in patients with insulin dependent (type 1) diabetes mellitus (n = 15); in patients with non-insulin dependent diabetes mellitus n = 15); and in healthy Nigerians (n = 252) from various tribal groups. In all three groups only commonly reported Bf allotypes namely BfF, F1, S and S1 were observed. More important, BfF1 allele was significantly increased in patients with insulin dependent (type 1) diabetes mellitus (expected 1/15, observed 5/15), X2 = P less than 0.005). It is suggested that this allele is probably the same as that reported in caucasoids and is part of a supratype or ancestral haplotype defined by HLA-B18, C4A3, C4A3, BQo, BfF1, DR3 marking type 1 (insulin dependent) diabetes mellitus.
The normal distribution in Northern Ireland of the genetic markers properdin factor B (Bf) and glyoxalase I (GLO) are described. These markers are available for comparison in disease studies, family studies and paternity studies.
Properdin factor B (Bf) phenotyping was carried out in 392 patients with rheumatoid arthritis (RA) and in 360 controls. In RA there were increased frequencies of both the Bf*S gene (83 vs 78%; pc = 0.0003) and the BfSS genotype 73 vs 61%; pc = 0.0002) and reduced frequencies of the Bf*F1 gene (0.5 vs 2.2%; pc = 0.03) and the BfFS genotype (20 vs 29%; pc = 0.0007). The frequencies of Bf*S in DR4 positive and DR4 negative RA were similar so that the findings were not accounted for by linkage disequilibrium between DR4 and Bf*S.
In a comparative study the presently known eleven allotypes of properdin factor B (Bf) were examined. Bf polymorphism consists of the two common alleles F and S, the two less common alleles F 1 and S 1 and seven further rare alleles. A variant designation has been proposed according to their relative electrophoretic mobility in comparison to the migration difference between the S and F 1 band. There rare variant alleles were redesignated: F 1.55, SO.45 and SO.7, which previously had been described as F 1.6, S 0.8 and S 1, respectively. Conversion studies did neither reveal variant mobility in the Bb nor in the Ba fragment of factor B in three of the rare alleles. This finding confirms the earlier report on one of the variants, possibly suggesting the existence of a so far unknown third clearing fragment.
Three different population samples have been tested for properdin factor B markers: 395 individuals from Schleswig-Holstein (Germany), 343 individuals (Europids) from Southern Brazil, and 309 individuals (Negroids) from Guinea-Bissau (Western Africa). These samples are showing marked differences in the distribution of Bf gene frequencies. As for the sample from Southern Brazil the Bf data are confirming the assumption that the Caucasoid population in Southern Brazil is somewhat mixed with Negroids.
Seventy-nine cases of Caplan's lung were typed for HLA-A and B antigens. The antigen Bw45 was present only in those patients with rheumatoid factor and was of significantly higher frequency (13.6%) when compared to a non-coal dust exposed population of 316 (1.0%). Those patients without rheumatoid factor showed an increase in HLA-A1 and B8 (58.6% and 51.7% respectively) when compared to the rheumatoid factor positive group (29.6% and 25.0% respectively). Clinical and radiological reassessment were performed on 49 of these patients who were also typed for HLA-DR antigens and properdin factor B allotypes. HLA-DR4 was raised in the rheumatoid factor positive group with rheumatoid arthritis (55.2% compared to 25.8% in the non-coal dust exposed group and 37.3% in coalworkers with normal radiographs). The HLA-DR results are comparable to those found in other studies of rheumatoid arthritis not associated with pneumoconiosis. The findings for HLA-A1, B8 and DR4, however, were not significant after correction was made for the number of antigens tested for. No particular Bf allotype was found to be associated with either the lung change or the arthritis. The induction of the pulmonary lesion in Caplan's syndrome is discussed in relation to the HLA findings.
The genetic polymorphism of properdin factor B(Bf) was first investigated in the Han population in Chengdu by isoelectrofocusing and immunofixation. The results revealed BfSS (129 cases), BfFS (48 cases) and BfFF (9 cases). No Bf variants were noted in this study. The allele frequencies were: Bf * S 0.8226, Bf * F 0.1774.
The genetic polymorphism of vitamin D binding protein (DBP) and of properdin Factor B (BF) was determined in unrelated Namibian San and Khoi, and in South African Blacks, Caucasoids and Cape Coloureds. Alleles have been confirmed by segregation patterns in family studies. The DBP phenotypes were identified by isoelectric focusing on ultrathin polyacrylamide gels and the BF phenotypes were identified by electrophoresis on 1% agarose gels; both methods were followed by immunofixation. The DBP and BF allele frequencies for all population groups were found to be in accordance with Hardy-Weinberg equilibrium. DBP*1S and BF*S allele frequencies in the San, Khoi and Blacks were similar; their frequency was far lower than in Caucasoids. The frequencies of the DBP*1F and BF*F were also similar in the San, Khoi and Blacks; however, the allele frequency was much higher in these groups than in Caucasoids. These differences were statistically significant (P < 0.001).
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