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Reunion Phenotype Am J Hum Genet 35:484-496, 1983 H-Deficient Blood Groups of Reunion Island. II. Differences between Indians (Bombay Phenotype) and Whites (Reunion Phenotype) JACQUES LE PENDU,' GILBERT GERARD,2 DIDIER VITRAC,3 GENEVIEVE JUSZCZAK,4 GENEVIEVE LIBERGE,4 PHILIPPE ROUGER, CHARLES SALMON,4 FRANCINE LAMBERT,' ANNE-MARIE DALIX,' AND RAFAEL ORIOL' SUMMARY Two variants of recessive, H-deficient nonsecretor individuals (h/h, sel se) were identified on Reunion Island: (1) H-negative individuals cor- responding to the classical Bombay phenotypes (Oh0, OhA, OhB, OhAB) who lack completely the H antigen on their red cells; all of them were Indian and had strong anti-H antibodies reacting with normal 0 and Oh red cells from whites; and (2) H-weak individuals (Oh, Ah, Bh, ABh). This phenotype represented the majority (85%) of the H-deficient phenotypes on Reunion Island, and all of them were white. They had only a weak expression of the H antigen and showed small but detectable amounts of ABH antigens on their red cells. Their anti-H antibodies reacted with normal 0 erythrocytes, but failed to react with Oh red cells, regardless of the ethnic origin of the donor. They were all from the same geographical area on the Island (Cilaos) and showed homogeneous titers of anti-H antibodies in sera. We propose to call this particular variant of weak H phenotype, belonging to the so-called para-Bombay series, Reunion. INTRODUCTION Two main types of recessive H-deficient red cell phenotypes may be defined according to the genetic model [1] proposing that Se and H are closely linked structural genes: (1) the nonsecretor classical Bombay type (h/h, selse) [2], H- Received June 8, 1982; revised July 13, 1982. This study was supported by CRL 811043, INSERM U20 and U76, and CNRS LA 143. Institut d'Immuno-Biologie, HFpital Broussais, 75674 Paris Cedex 14, France. 2 Centre de Transfusion, H6pital Bellepierre, 97405 St-Denis, La R6union. Poste de Transfusion, H6pital St-Pierre, 97448 St-Pierre, La Rdunion. 4 CNTS, H6pital St-Antoine, 75571 Paris Cedex 12, France. C 1983 by the American Society of Human Genetics. All rights reserved. 0002-9297/83/3503-0013$02.00 484 H-DEFICIENT BLOOD GROUPS 485 deficient for both red cells and saliva, and (2) the secretor Bombay type with normal ABH in secretions but H-deficient for erythrocytes (h/h, Sel-) [3]. Bombay nonsecretors, the first type, have been shown to be heterogeneous [4, 5]. Some lack the H antigen completely. They have normal A or B enzymes in sera according to their ABO genotype OhA, OhB, OhAB), but their apparent red cell phenotype is always 0h. Other H-deficient individuals have only a weak expression of H. They have small amounts of H on erythrocytes that are transformed into A or B antigens and can be detected by direct agglutination or fixation-elution tests in A, B, or AB individuals and, consequently, have Ah, Bh, or ABh phenotypes. Although, theoretically, Oh with 0/0 genotype and weak expression of H should have small amounts of H and should be different from the 0h with complete lack of H, the difference between these two variants of Oh is difficult to ascertain. In practice, the heterogeneity of Oh phenotypes suggests that several weak alleles of H [6, 7] might exist, and therefore the H-h system could have a large quantitative polymorphism instead of the dimorphic H-h model classically accepted (reviewed in [8]). In accordance with this concept, Moores et al. [9] proposed the existence of at least two kinds of Oh phenotypes, since the 0h individuals from the Indian community of Natal were completely negative for ABH antigens, even with the most sensitive adsorption-elution tests. This was in contrast to other European reports showing some 0h phenotypes to have small amounts of erythrocyte ABH antigens detectable only by adsorption-elution tests [10-12]. The existence of the H-deficient phenotype on Reunion Island has been known for more than 10 years [13, 14], and a series of 42 H-deficient nonsecretor individuals has been reported recently [15]. The great majority of these phenotypes belong to the so-called para-Bombay group (Ah, Bh, and ABh). However, more detailed family studies described here suggest that at least three 0h individuals had normal A and/or B enzymes in sera but did not have detectable A and/or B antigens on red cells and were, consequently, OhA, OhB, and OhAB, respectively. Thus, two variants with complete and partial suppression for the expression of ABH antigens on red cells can be distinguished among the recessive H-deficient nonsecretor phenotypes of Reunion Island. Furthermore, quantitative analysis of ABH antigens on red cells and the reactivity of their anti-H antibodies showed a new and unexpected association between the amount of H antigen expressed on red cells and the ethnic origins (Indian or white) of the H-deficient individuals from Reunion Island. Indian H-deficient individuals were completely negative for the H antigen, while white H-deficient individuals had a weak, but positive, H antigen. In addition, the small amounts of H antigen produced by these white, weak H phenotypes were recognized by the anti-H antibodies of the H-deficient Indian individuals. MATERIALS AND METHODS The main reagents used for blood typing of the H-deficient subjects and their families were: Plant lectins Ulex europaeus whole extract was obtained from CNTS (Paris, France); Ulex europaeus lectin 1, purified by affinity chromatography, was obtained from Pharmindustrie IBF 486 LE PENDU ET AL. (Villeneuve-la-Garenne, France); Dolichos biflorus whole extract was obtained from CNTS; Bandeiraea simplicifolia lectin 1, purified by affinity chromatography, was obtained from E-Y Laboratories (San Mateo, Calif.). Animal Reagents Eel sera (anti-H), Helix pomatia extract (anti-A), and sheep hyperimmunized sera (anti- B) were obtained from CNTS. Human Antisera Human anti-A, and anti-B, and anti A+B were of immune origin and provided by CNTS. Anti-AI was obtained from an A2B individual. They were identified with the first four letters of the blood donor's surname. Papain Treatment of Erythrocytes One vol of washed red cells was incubated for 7 min with 1 vol of papain solution (Prolabo, Paris, France) in phosphate-buffered saline containing 1 mg/ml of cysteine [16]. Agglutination Tests were performed with native red cells (tests for identification of A,, A2, B, and H antigens) or papain-treated red cells (tests with sera of Oh donors). In each case, the tubes with 50 ,Il of the twofold serial dilutions of the reagents were incubated with 50 RIJ of a 5% suspension of erythrocytes for 1 hr at room temperature (20'C + 20C). The microag- glutination was observed with a microscope, and results were expressed in terms of cu- mulative scores ( + ++ = 10, + + = 8, + = 5, (+) = 2, - = 0) [16]. Immunoadsorbents Synthetic H type 1 and H type 2 trisaccharides bound to a solid matrix of crystalline silica were obtained from Chembiomed (University of Alberta, Edmonton, Canada). Glycosyltransferase Activity in Sera The A and B enzymes were measured by incorporation of N-acetyl [14C] galactosamine and [14C] galactose on 2'-fucosylactose, respectively [17, 18]. A1 and A2 enzymes can be distinguished by their isoelectric points [19] and by their optimum pH activity [17]. The ratio of A-enzyme activity at pH 6.0 and pH 7.0 was used to determine the A, or A2 character of the A enzyme present in sera of two H-deficient individuals (see legends of figs. 4 and 5). RESULTS White Pedigrees Forty-two H-deficient nonsecretor individuals, belonging to 25 different ped- igrees, were found on Reunion [15]. Twenty-one of these 25 families (85%) were white, and H-deficient individuals with at least one A and B gene expressed small amounts of the corresponding A or B antigens on their red cells (i.e., the two largest pedigrees of this series had two Ah, three Bh, and two ABh individuals [15]. Other examples of Reunion H-deficient white pedigrees are shown in figures 1-3. The CAD. family (fig. 1) has three H-deficient siblings, but the proposita (11-8) is Oh while her two H-deficient sibs (II-4 and II-10) are Bh. The sera of II- 8 had no glycosyltransferase activity, confirming that she had inherited 0 genes H-DEFICIENT BLOOD GROUPS 487 I. 1 20 0 Se Le II. 1 2 3 4 5 6 7 8 9 10 11 12 13 l 6 6 6 -{ 6 B B Bh B 0 °h B Bh B B Se Se se Se Se Se se se se Se Se Le Le Le Le Le Le Le Le Le Le Le III. 1 2 3 4 5 6 7 8 9 10 11 12 1314 15 16 17 18 19 20 21 B OO O O B OO B B O0O B 00 0 Se so Se se se Se se Se se Se se se se se se se se se se Le Le Le Le Le Le Le Le Le Le le Le le le Le Le le Le Le FIG. 1.-CAD. pedigree. White with weak expression of H antigen. Three H-deficient siblings were found (II-4, -8, -10). Erythrocytes of II-4 and 11-10 were agglutinated by anti-B (table 1), and normal B glycosyltransferase activity was found in their sera. Erythrocytes of II-8 were not agglutinated by anti-B, and there was no B glycosyltransferase in her serum. Offspring of II-8 x II-9 were nonsecretors (selse) as predicted by model proposed in [1].
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