A second Dr(a−) proposita with anti‐Dr<sup>a</sup> and a family with the Dr(a−) phenotype in two generations

Levene, C.; Harel, Noam; Kende, G.; Papo, S.; Bradford, Matilda; Daniels, Geoff

doi:10.1046/j.1537-2995.1987.27187121478.x

Cited by 28 publications

(18 citation statements)

References 3 publications

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“…Dr(a-) erythrocytes showed reduced hemagglutination with antibodies to non-Dra Cromer-related blood group antigens (30,31), suggesting a reduced level of all Cromer-related antigens and hence of DAF. To confirm this directly, a radioimmunoassay was used to measure the levels of anti-DAF reactivity with Dr(a+) and Dr(a-) erythrocytes.…”

Section: Resultsmentioning

confidence: 99%

Dr(a-) polymorphism of decay accelerating factor. Biochemical, functional, and molecular characterization and production of allele-specific transfectants.

Lublin¹,

Thompson²,

Green³

et al. 1991

J. Clin. Invest.

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The Dr' antigen belongs to the Cromer-related blood group system, a series ofantigens on decay accelerating factor (DAF), a glycosyl-phosphatidylinositol-anchored membrane protein that protects host cells from complement-mediated damage. We studied the rare inherited Dr(a-) phenotype to ascertain the associated biochemical and functional changes in DAF and to characterize the basis for this polymorphism. Radioimmunoassay and flow cytometric analysis ofDr(a-) erythrocytes demonstrated 40% of normal surface expression of DAF but normal levels of several other glycosyl-phosphatidylinositol-anchored proteins, distinguishing this phenotype from that of paroxysmal nocturnal hemoglobinuria. Western blots confirmed this reduced DAF expression and indicated a slightly faster mobility of the molecule on SDS-PAGE. Despite the reduced DAF expression, Dr(a-) erythrocytes functioned normally in the complement lysis sensitivity assay. Utilization of the polymerase chain reaction to amplify mononuclear cell genomic DNA from three unrelated Dr(a-) individuals demonstrated that a point mutation underlies the Dr(a-) phenotype: a C to T change in nucleotide 649 resulting in a serine'65 to leucine change. This defines the Drb allele ofDAF, which can be distinguished from Dr' by a Taq I restriction fragment length polymorphism. We created transfected Chinese hamster ovary cell lines expressing either the Dr' or the Dr' allelic form of DAF.These allele-specific transfectants were tested by inhibition of hemagglutination or flow cytometry and confirmed the specificity of anti-Dr' alloantisera. The allele-specific transfectants could form the basis of a new serological approach to immunohematology. (J. Clin. Invest. 1991.87:1945-1952

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Section: Resultsmentioning

confidence: 99%

Dr(a-) polymorphism of decay accelerating factor. Biochemical, functional, and molecular characterization and production of allele-specific transfectants.

Lublin¹,

Thompson²,

Green³

et al. 1991

J. Clin. Invest.

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“…One of the 4 sibs of the original Dr(a-) proposita [5] was also Dr(a-). In the second family [6] the proposita had no Dr(a-) sib, but 3 of her 4 children were Dr(a-). In the third family [C. Levene and S. Kaufman, personal com munication] 3 of the 4 sibs of the proposita were Dr(a-).…”

Section: Cromermentioning

confidence: 99%

Cromer-Related Antigens - Blood Group Determinants on Decay-Accelerating Factor

Daniels¹

1989

Vox Sanguinis

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Cromer-related antigens, a series of blood group antigens phenotypically related to each other through various serological characteristics, have recently been shown to be carried on the complement regulatory glycoprotein decay-accelerating factor (DAF). Cromer-related antigens, therefore, represent a number of inherited variants and polymorphisms of DAF. The Inab phenotype, a ‘Cromer-null’ phenotype in which the red cells lack all Cromer-related antigens, appears to be an inherited DAF deficiency.

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“…Despite the reduced DAF expression, Dr(a–) erythrocytes function normally in the complement lysis sensitivity assay [6]. The inherited Dr(a–) phenotype has been found in Israel only in 4 families who immigrated from the area of Bukhara [7, 8]. The red cells of these patients lacked the high incidence Drori antigen Dr a and had a weakened expression of the Cr a , Tc a , and IFC antigens.…”

Section: Discussionmentioning

confidence: 99%

“…Dr a has been shown to be the receptor for the fimbria-like adhesion of the 075X-positive Escherichia coli that agglutinate all red cells except those which are Dr(a–) and those of the Inab phenotype (not expressing the Cromer-related antigens) [9]. The Dr a blood group substance is present in serum [8] and has been found in the tubular basement membrane and Bowman’s capsule of the human kidney [9]. Prior to transplantation, the kidney graft was perfused with cold preservation solution to reduce donor blood to a minimum.…”

Section: Discussionmentioning

confidence: 99%

Dr<sup>a</sup> (Cromer-Related Blood Group Antigen)-Incompatible Renal Transplantation

Nakache

Levene²,

Sela³

et al. 1998

Vox Sanguinis

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Background and objectives: Cromer system antigens, a series of blood group antigens of very high frequency, are not considered to be clinically significant in transfusion. In renal transplantation only the ABO blood group antigens are considered essential. The Drori blood group antigen is present in serum and has been found to reside on the renal tubular basement membrane and Bowman’s capsule. The effect of anti-Dr^a on the renal parenchyma has not been evaluated. Materials and methods: A unique case of renal transplantation of an incompatible Dr(a+) kidney to a Dr(a–) patient with anti-Dr^a in her serum is presented. Results: Graft function was immediately good. The titer of anti-Dr^a remained unchanged following transplantation. Conclusion: The successful outcome of a case of a Drori (Dr^a)-incompatible kidney transplantation confirmed the lack of clinical significance of the anti-Dr^a relating to transplantation.

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A second Dr(a−) proposita with anti‐Dr^a and a family with the Dr(a−) phenotype in two generations

Cited by 28 publications

References 3 publications

Dr(a-) polymorphism of decay accelerating factor. Biochemical, functional, and molecular characterization and production of allele-specific transfectants.

Dr(a-) polymorphism of decay accelerating factor. Biochemical, functional, and molecular characterization and production of allele-specific transfectants.

Cromer-Related Antigens - Blood Group Determinants on Decay-Accelerating Factor

Dr<sup>a</sup> (Cromer-Related Blood Group Antigen)-Incompatible Renal Transplantation

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A second Dr(a−) proposita with anti‐Dra and a family with the Dr(a−) phenotype in two generations

Cited by 28 publications

References 3 publications

Dr(a-) polymorphism of decay accelerating factor. Biochemical, functional, and molecular characterization and production of allele-specific transfectants.

Dr(a-) polymorphism of decay accelerating factor. Biochemical, functional, and molecular characterization and production of allele-specific transfectants.

Cromer-Related Antigens - Blood Group Determinants on Decay-Accelerating Factor

Dr<sup>a</sup> (Cromer-Related Blood Group Antigen)-Incompatible Renal Transplantation

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A second Dr(a−) proposita with anti‐Dr^a and a family with the Dr(a−) phenotype in two generations