Bloods from three individuals, one each of the phenotypes Oh-A, Oh-B and Oh-O have been studied. The work of Dzierzkowa-Borodej, et al.-10 was confirmed when it was shown that all three samples of Oh red blood cells had increased I antigen strength. The i, Sd-a, Le-a and Le-x antigens were not found to be increased. Attempts were made to adsorb and elute anti-A, anti-B and anti-A,B with the Oh red blood cells, using sera that contained high titered anti-I antibodies. This was done in the belief that previously reported positive results in such tests might be due to the high level of I on the Oh red blood cells, anti-I in the sera containing the ABO antibodies, and the Matuhasi-Ogata phenomenon. However, in no instance were we able to adsorb an ABO antibody onto the Oh red blood cells. Contrary to the report of others-10 the titers of anti-A, anti-B and anti-H in the sera of the three Oh individuals studied did not differ significantly. We suggest that the evidence from our findings and the work of others is sufficient to show that at least two forms of the Oh phenotype exist: one representing total suppression of H, A, and B antigens, and the other marked but not total suppression, with partial inhibition of antibody production.

ABO Blood-Group System↗

PubMedDate not supplied

Successful transfusion of Chido-positive blood to two patients with anti-Chido.

Two cases are described in this report in which patients with anti-Chido in the serum were transfused with Chido-positive blood. Since there was evidence of normal survival of the transfused red blood cells, these findings do not support a suggestion that patients with anti-Chido may require transfusion with Chido-negative blood. In spite of the apparently normal survival of the Chido-positive blood, a previous report in which it was shown that weakly Chido-positive blood can stimulate the production of anti-Chido was confirmed.

Aged↗

PubMedDate not supplied

An autoantibody with anti-Wrb specificity in a patient with warm autoimmune hemolytic anemia.

A patient with warm autoimmune hemolytic anemia (AIHA) has been found to possess an autoantibody with Wrb specificity. While this is the first known description of Wrb specificity in this disease, additional studies on the Wrb status of En(a-) cells indicate that autoantibodies previously thought to be anti-Ena are in reality also anti-Wrb. Autoantibodies with Wrb specificity may thus be a rather common finding in patients with AIHA who have been thought to have "panagglutinins" on their red blood cells. Since anti-Wra alloantibodies are found frequently in patients with AIHA, it seems possible that the Wright system holds some clue to the pathogenesis of this disease.

Anemia, Hemolytic, Autoimmune↗

PubMedDate not supplied

An En(a-) red cell sample that types as Wr(a-b-).

In the course of investigating a patient with autoimmune hemolytic anemia in which the causative autoantibody had anti-Wrb specificity, it was demonstrated that an En(a-) red blood cell sample typed as Wr(a-b-). The only known example of Wr(a+b-) blood typed as En(a+) so that anti-Wrb and anti-Ena do not have the same specificity.

Anemia, Hemolytic, Autoimmune↗

PubMedDate not supplied

A new example of anti-LW and further studies on heterogeneity of the system.

A case is reported in which an LW3 woman formed anti-LW. It is shown that the case represents the "genetic" and not the "transient" type of red blood cell LW antigen depletion. Studies have confirmed the quantitative difference of LW antigen on LW3 and LW4 red blood cells and the fact that Rhnull individuals produce the only totally LW-negative red blood cells. The difficulties encountered in the identification of anti-LW, because of the LW3 and LW4 states, are described. It is clear, from this study, that if random donors are typed for LW using anti-LW made by an LW4 indvidual, those who are LW3 will be classed as unremarkable LW-positives.

Adsorption↗

PubMedDate not supplied

The phenotypes En(a-), Wr(a-b-), and En(a+), Wr(a+b-), and further studies on the Wright and En blood group systems.

In 1975, we showed 18, 19 an En(a-) blood sample to be phenotypically Wr(a-b-). In the current report, we describe tests that show that three En(a-) members of a single family, not believed to be related to the family of the previously tested En(a-) person, are also Wr(a-b-). They have red blood cells that neither react with nor adsorb anti-Wra or anti-Wrb. In addition, we have shown that the red blood cells of six EnaEn heterozygotes, in the family tested, are Wr(a-b+) but carry only a single dose of Wrb antigen. Tests on anti-Ena have shown conclusively that one example is a mixture of separable anti-Ena and anti-Wrb and that a second example may well contain the same two antibodies. By various methods, we have demonstrated that the red blood cells of the only known Wr(a+b-) individual are En(a+) and do not display any of the physicochemical abberations of the En(a-) phenotype. It is further shown that neuraminidase and trypsin do not denature the Wra or Wrb antigens in vitro, but that the protease ficin does have a limited ability to denature Wrb. Additional observations on the first reported example of anti-Wrb are included. These various findings have been considered in the light of gene linkage of, or gene interaction between, the En and Wright system genes. It is concluded that the evidence does not exclude the possibility that En is a silent allele at the WraWrb locus so that the genotype EnEn (or WrWr) might result in the phenotype En(a-), Wr(a-b-). However, it is also pointed out that the evidence equally well supports the postulation that the Wra and Wrb genes are unable to function in the absence of an Ena gene. If this latter theory is proved correct, the interaction between Ena and the Wright genes can be thought of as similar to that between the H and ABO or X1r and CDE genes. It is pointed out that if En is a silent allele at the MN locus (current evidence on this point is not conclusive,) En and Wr cannot be synonymous for it is known that the Wra and M and N genes segregate independently. Location of En at the MN locus would not, however, refute the theory that Wra and Wrb cannot function in the absence of En. Finally, it is pointed out that the supposed anti-Wrb is probably just what its name implies but that even if this assumption is later disproved, the high incidence antigen defined by the antibody presently called anti-Wrb is unequivocally associated with Ena.

Blood Group Antigens↗

PubMedDate not supplied

Independence of Wright from many other blood group systems.

The finding that En(a-) red blood cells are Wr(a-b), and thus probably represent a "null" phenotype of the Wright system, has provided evidence of the independence of the Wright blood group system from many others. Detection of blood group antigens on "null" red blood cells almost certainly indicates that those antigens do not belong to the same blood group system as the "null" cells. In the case of Wright, lack of certainty that En(a-) is the "real", or only, null type slightly reduces the weight of the evidence.

Blood Group Antigens↗

PubMedDate not supplied

Autoantibodies mimicking alloantibodies.

A patient with myelofibrosis, who has produced many red blood cell autoantibodies, is described. Although the patient is phenotypically R1R1 (CDe/CDe), eluates made from his red blood cells have consistently contained what appeared to be anti-E, and more recently another antibody that appeared to be anti-c. In in vitro experiments we have shown that the "anti-E" and "anti-c" can be totally adsorbed by E-negative and c-negative red blood cells, respectively. We conclude that the two antibodies have quite different specificities from those indicated by simple antibody identification studies, and that both are more closely related to the anti-Hr series of antibodies than to anti-E or anti-c.

Adsorption↗