A Second Example of —/— or Rh<sub>null</sub> Blood

Levine, Philip; Celano, Marino; Falkowski, F.; Chambers, Jane; Hunter, Oscar B.; English, Carol T.

doi:10.1111/j.1537-2995.1965.tb01193.x

Cited by 55 publications

(22 citation statements)

References 10 publications

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“…Flowever, the finding that -D-red cells react weakly with anti-Fy5 is another reason for believing that it is the Rh genes that are involved. All 4 Rhnuii samples available to us were of the aboriginal variety, in which homozygosity for X°r genes prevents expression of the Rh genes [8].…”

Section: Discussionmentioning

confidence: 99%

Anti-Fy5, an Antibody Disclosing a Probable Association between the Rhesus and Duffy Blood Group Genes

Colledge

Pezzulich

Marsh³

1973

Vox Sanguinis

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A new antibody, anti-Fy5, has been found in the serum of a Negro Fy(a-b-) person. It reacts with Fy(a+) or Fy(b+) red cells of common Rh type, but not with Fy(a-b-) cells from Negroes, or with Rh(null) cells. An example of Caucasian Fy(a-b-) red cells was Fy5 positive. U-negative or LW-negative red cells give the reaction expected of their Duffy type. The data suggest that the Fy5 determinant is formed by interaction of Rhesus and Duffy gene products.

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Section: Discussionmentioning

confidence: 99%

Anti-Fy5, an Antibody Disclosing a Probable Association between the Rhesus and Duffy Blood Group Genes

Colledge

Pezzulich

Marsh³

1973

Vox Sanguinis

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“…The 33 qualitatively different antigenic specificities of the Rh blood-group system (1, 2) have become extraordinarily difficult to organize systematically. Each allele at the Rh locus determines a variable number of different antigens (3,4), and recombination has been observed in just one family (5).…”

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confidence: 99%

“…A main point of regulation, although not an absolute necessity, clearly indicates how all of Rh is susceptible to suppression, especially by independently segregating, partially recessive genes. The known independent suppressors are called X~r (33) and XQ (34) although neither is associated with the X chromosome. Both have profound effects when homozygous: X~r/X~r produces Rhnull (33) in which no Rh antigens are expressed, while XQ/XQ depresses slightly less and produces "pseudo rhG" (34).…”

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confidence: 99%

“…The known independent suppressors are called X~r (33) and XQ (34) although neither is associated with the X chromosome. Both have profound effects when homozygous: X~r/X~r produces Rhnull (33) in which no Rh antigens are expressed, while XQ/XQ depresses slightly less and produces "pseudo rhG" (34). Furthermore, all known examples of either blood type are associated with congenital hemolytic anemia characterized by cup-shaped erythrocytes (stomatocytes) rather than normal discoid erythrocytes (35,36).…”

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confidence: 99%

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Genetic Model for the Rh Blood-Group System

Rosenfield

Allen

Rubinstein

1973

Proc. Natl. Acad. Sci. U.S.A.

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Inherited quantitative aspects of the Rh blood-group system and susceptibility of Rh to the effects of independently segregating suppressor genes can be accounted for with a conjugated operon model. This assumes the existence of four operator or promotor (control) genes for these functions, while closely linked structural regions determine the qualitative characteristics of Rh antigens. Observed restriction of antigenic crossreactivity to the products of adjacent genetic regions and data from blood typing of nonhuman primates both suggest that Rh complexity arose from a series of gene duplications and independent mutations.The 33 qualitatively different antigenic specificities of the Rh blood-group system (1, 2) have become extraordinarily difficult to organize systematically. Each allele at the Rh locus determines a variable number of different antigens (3,4), and recombination has been observed in just one family (5). In addition, quantitative differences in the expression of Rh antigens are also under the control of Rh genes (6). Accommodation of quantitative data by genetic theories devised to account only for qualitative alloantigenic variants (3,4,7,8) results in a vast increase in an already overwhelmingly large number of complex alleles.In this report, Rh data have been arranged in a manner that distinguishes qualitative from quantitative information. From this arrangement, a consistent genetic model emerges that may provide a biologically sounder conceptual basis for this complex system.In the Rh system (see Table 1 for glossary of terms) Rh: wl (Rh or DU) was the first quantitative variant found (9). A most interesting situation was shown to involve allelic interaction, with the R-",2 -3 (r' or dCe) gene being suppressive of RI alleles (R or D) in trans position (10). Quantitative variants of RI were documented quantitatively by Silber et al. (11) and Masouredis (12), but Gibbs and Rosenfield (6) found that the quantitative "degree of expression" was under the strict genetic control of Rh genes and so was the interallelic depressive effect of R-1"2 -3. Within an extensive pedigree, identical genotypes were quantitatively identical for four different Rh antigens, whereas qualitatively similar genotypes in the general population varied over a significant range (6). Using a different method, Berkman et al. (13) confirmed these observations and extended the findings to the other blood groups.

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“…It is believed to arise in one of two ways : (a) inheritance from both parents of the independent modifying gene X°r which prevents expression of Rh [3] and (b) inheritance from both parents of an amorphic allele at the Rh locus [2],…”

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confidence: 99%