The r' gene is overrepresented in hrB-negative individuals.

A screening program was implemented to identify hrB- donors. D- C+, D-C-, and D+C- samples from African-American donors were typed with multiple examples of anti-hrB and anti-hrB-like, and one example each of anti-V and anti-VS. Of 75 D-C+ donors, 4 (5%) typed as hrB-, and 14 others had weak or variable expression of hrB. Of these 18 individuals, 15 were V-VS+, and 3 were V+VS+. No hrB- sample was found in 90 C- donors, 26 of whom were V+VS+, and 1 was V-VS+. A review of our records of 44 hrB- patients and donors studied earlier revealed that at least 12, and possibly as many as 30, carried r or rs. All hrB- donors found in our screening program had D-C+VS+ RBCs, indicating an overrepresentation of r. Our record review also showed that the presence of r and rs more often results in hrB- RBCs, and that the most effective way to screen for hrB- donors is to type African Americans who have D-C+ RBCs.

First example of Rh:-32,-46 red cell phenotype.

The red cells of a white male blood donor typed as Rh:-1, -2, -3,w4,w5,6,-17,w19,-31,-32,-34, and -46. Although the donor has no history of transfusion, his serum contains an alloantibody that is weakly reactive with most red blood cells (RBCs) tested. Only Rhnull and D-- RBCs are nonreactive. Reactivity is enhanced with ficin- or papain-treated RBCs and is unaffected by AET or DTT treatment of the RBCs. Previously described Rh:-46 RBCs have been of deletion types D--, D, and Rhnull, or Rh:32. In three multitransfused patients, the Rh46 antigen was temporarily suppressed and the phenotype eventually reverted to normal. This is the first report of RBCs of the Rh:-32,-46 phenotype that are not of a rare Rh deletion or Rhnull type. In addition, the Rh:w5,w19,-31,-34 phenotype is rarely found in whites.

Race-related red cell alloantibody problems.

Some years ago differences in red cell blood group phenotypes among individuals of different ethnic backgrounds were of little moment to blood transfusion services. This was because in many instances the ethnic group of the majority of patients closely matched that of the donor pool. The dramatic population movements of the last 20-30 years have changed this situation. Now it is not uncommon for a transfusion service whose donors are primarily European Caucasian in ancestry to be required to supply blood for patients, a substantial proportion of whom are of Black or Oriental extraction. This problem affects the donor service in terms of supply and demand, and both the donor service and hospital transfusion service in terms of antibody identification. In this paper some aspects of this problem are explored and illustrations are given of how knowledge of an antibody-maker's ethnic background can sometimes be used to accelerate identification of an antibody, particularly one directed against a very common antigen. The effects of differences in antigen frequency are also considered in terms of long-term transfusion support of some patients.

Autoimmune hemolytic anemia and cold hemagglutinin disease: clinical disease and laboratory findings.

As is apparent from the length of this review, a multitude of laboratory investigations can be performed on the blood of patients with AIHA and CHD. Unfortunately, because of the considerable complexity of some of these tests, their significance is not always apparent to the physician who treats the patient. Communication gaps between the laboratory scientist and the physician at the bedside are bound to occur because of the high degree of specialization of both immunohematology and medical care. The purpose of this review has been to bridge the communication gap. The agents that cause AIHA and CHD are antibodies. Although they are often autoantibodies of complex specificity, usually reacting with all normal red cells, they nevertheless obey most of the rules explaining the action of alloantibodies that sometimes complicate transfusion therapy. By approaching AIHA and CHD as antibody-induced conditions, and by regarding autoantibodies as similar in their actions to alloantibodies, hopefully, physicians will appreciate the significance of the tests performed in the laboratory. For their part, the laboratory workers will be able not only to report test results but also to explain the findings. This review may aid in establishing the essential dialogue.

Anticomplement and the indirect antiglobulin test.

We used 140 IgG complement-fixing blood group alloantibodies of 17 different specificities in tests to determine whether anticomplement antibodies are still necessary in antiglobulin reagents to be used in indirect antiglobulin tests. Anti-Rh and other IgG noncomplement fixing antibodies were excluded from the study. A polyspecific antiglobulin reagent that contained anti-IgG and anticomplement antibodies, and an anti-IgG reagent containing the same level of anti-IgG as the polyspecific one, were compared. Titrations with some of the antibodies were repeated with only the polyspecific reagent. With each antibody, studies were done with complement activation blocked, and compared with results in which it was allowed to proceed. We found that 42.9% of the antibodies were detected at a higher dilution, and 64.3% of them were detected with a higher titer score, when the poly-specific antiglobulin serum containing anticomplement antibodies was used. We conclude that anticomplement antibodies are indeed still essential for the correct performance of indirect antiglobulin tests.

Notes on the Ena and U antigens of Ena(En.OP) heterozygotes, and the U antigen of En(a--) individuals.

Using two anti-Ena antibodies, from which anti-Wrb had been removed, and anti-U antibodies, the authors have failed to demonstrate any difference in the amounts of Ena and U antigens on the red blood cells of individuals with one and two functioning Ena(En.OP) genes. Two En(a--) samples, one from an individual who is En/En (En.op/En.op) and the other En/Mk (En.op/Mk), could not be distinguished from U-positive samples from individuals with two functioning U (U.OP) genes in dosage studies with anti-U.

Anti-Tm is anti-N polypeptide.

Anti-Tm defines an antigen in the MN blood group system, and 382 Tm + samples were found in tests on 900 random Caucasian, and 500 random Negro bloods. Of the 382 Tm + samples, 373 were also N +, but a further 625 N+ samples were nonreactive with anti-Tm. We have now shown that when the original anti-Tm serum is adsorbed free of anti-T, and is tested against neuraminidase-treated red blood cells, it has anti-N specificity. Further, while anti-Tm cannot be inhibited by sialoglycoprotein (SGP) preparations from untreated N+ red blood cells, it is inhibited by SGP fractions prepared from N+ red blood cells that have been pretreated with neuraminidase. It seems that anti-Tm is directed against a part of the polypeptide backbone of the N SGP.

Further studies on the dependence of some examples of anti-M and anti-N on the presence of red-cell-borne sialic acid.

Previous studies have shown that some examples of anti-M and anti-N fail to agglutinate neuraminidase-treated (NeuNAc-depleted) red cells. This investigation extends those observations and shows that the antibodies fail to bind to such treated red cells. These observations may mean that NeuNAc residues act to orient the protein portion of the MN sialoglycoprotein so that it is recognized by the antibodies. Alternatively, it is possible that NeuNAc residues are an integral part of the antigen defined.

Critical re-examination of the specificity of auto-anti-Rh antibodies in patients with a positive direct antiglobulin test.

Forty-eight autoantibodies with apparent 'simple' anti-Rh specificity (anti-e, -E, -c, -D, -C, -Ce, -G), have been studied by means of multiple absorption tests. The finding that 34 (70.8%) of these antibodies could bind to red blood cells lacking the antigens that the antibodies appeared to define, indicated that the antibodies had different specificities than seemed to be the case in initial antibody identification tests. Those autoantibodies that at first appeared to be directed against the Rh antigens e, E or c, most often had anti-Hr or anti-Hro specificity. These data explain why some apparent anti-Rh autoantibodies can be eluted from the red blood cells of patients negative for the antigens that the antibodi:s appear to define. However, they also illustrate that the phenomenon of autoantibodies mimicking specificities that they do not possess is common in patients positive for the antigens against which their autoantibodies appear to be directed. An explanation for the mode of action of these autoantibodies in complexing with the Rh agglutinogen is proposed, and the significance of the antibodies in transfusion therapy is considered.