The Heterogeneity of Erythrocyte Antigen Distribution in Human Normal Phenotypes: an Immunoelectron Microscopy Study

Reyes, F; Gourdin, M F; Lejonc, J. L.; Cartron, Jean Pierre; Gorius, J. Breton; Dreyfus, B

doi:10.1111/j.1365-2141.1976.tb03608.x

Cited by 21 publications

(9 citation statements)

References 28 publications

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“…26,27 The mechanisms are unclear but are perhaps due to the weaker blood groups being associated with a different sequence in the upstream region. It has recently been shown that an upstream repeat element of the ABO gene, which varies in copy number according to the allele, has enhancing ability.…”

Section: Discussionmentioning

confidence: 99%

Loss of red cell A, B, and H antigens is frequent in myeloid malignancies

Bianco

Farmer

Sage

et al. 2001

Blood

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IntroductionThe A, B, and H antigens (hereafter referred to as ABH antigens) are complex carbohydrate structures found on glycoproteins and glycolipids present on the surface of erythrocytes, endothelial cells, and on most epithelial cells. Alleles of the ABO gene code for glycosyltransferases that act on the precursor H antigen. 1,2 In red blood cells, the H antigen is determined by a fucosyltransferase coded for by the FUT1 gene. If the H antigen is absent, there is no substrate for the ABO glycosyltransferases to modify. Homozygous deficiency of FUT1 gives rise to the Bombay phenotype where there are no A or B antigens on the red cell due to lack of the H precursor. The major alleles of the ABO gene are A, which adds N-acetylgalactosamine to give the A antigen; B, which adds galactose to give the B antigen; and O, which is a null allele coding for an inactive transferase incapable of modifying the H antigen. The most frequent of the minor A and B alleles is the A 2 allele, which gives rise to a lower density of A antigen. Weaker alleles such as A 3 and A x show progressively less A antigen. 3 Alteration of ABH antigens in hematologic malignancy was first reported by van Loghem et al, 4 who described very weak A antigen expression on the red cells of a patient with acute myeloid leukemia (AML), who had previously shown normal A antigen expression. Loss of A, B, or H antigens from the surface of red blood cells is now recognized as a recurrent observation in hematologic malignancy. 5,6 In a healthy individual of type A, B, or AB, complete agglutination of the red blood cells is observed after incubation with antibodies reactive against their blood group. In patients with loss of ABH antigens, a varying proportion of red blood cells do not agglutinate, giving a characteristic mixed-field reaction. Mixed-field reactions can also occur in healthy individuals where the reactions are associated with rare alleles of the ABO gene such as A 3 and B 3 .Loss of ABH antigens is also seen in the tumor cells of many types of carcinoma, including bladder, lung, head and neck, cervical, and thyroid, where it has been associated with tumor grade, metastatic potential, and poor prognosis. 7-13 Furthermore, laboratory studies have shown that tumorigenicity is reduced when A or B antigens are expressed. 14,15 Whether the mechanisms of loss of ABH antigens in epithelial tumors and hematologic malignancies are truly analogous to each other remains to be determined.Unlike epithelial malignancies where the loss of ABH antigens is seen in dedifferentiated tumor cells, loss of ABH antigens in myeloid malignancies is only seen on red cells as most hematopoietic cells and precursors do not express ABH antigens. However, malignant stem cells often retain the potential to differentiate along the erythroid lineage. [16][17][18] Thus, loss of ABO expression in the population of red cells derived from a malignant stem cell is an indicator of genetic changes that have occurred in the malignant stem cell. Consistent with this, Salmon et al 19 s...

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Section: Discussionmentioning

confidence: 99%

Loss of red cell A, B, and H antigens is frequent in myeloid malignancies

Bianco

Farmer

Sage

et al. 2001

Blood

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“…Even though we were cautious to avoid agglutination, RBC gates were drawn very tightly, based on side scatter/forward scatter to exclude clumped cells. The number of group O cells staining with lectin was always less than 0.5%; however, the number of group A 1 cells that did not stain with the lectin varied from 0% to 8% (because it was not possible to add excess lectin to ensure binding to all cells and because of differential expression of A 1 antigen 16 ). The small number of recipient A 1 cells that failed to bind lectin was not considered significant for our study because lectin binding was used only to positively identify group A 1 cells and to exclude group O cells.…”

Section: Flow Cytometrymentioning

confidence: 99%

Transfer of glycosylphosphatidylinositol-anchored proteins to deficient cells after erythrocyte transfusion in paroxysmal nocturnal hemoglobinuria

Sloand

Mainwaring

Keyvanfar

et al. 2004

Blood

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“…This was not correlated with either homo-or heterozygosity for the X chromosome, or with differences in maturity of peripheral blood granulocytes. The phe nomenon shows some analogy with the het erogeneous distribution of the A antigen over normal A erythrocytes [15]. The in teresting possibility that NBj is specific for a subpopulation of granulocytes must be further studied.…”

Section: Discussionmentioning

confidence: 99%

Serological, Immunochemical and Immuoncytological Properties of Granulocyte Antibodies

Verheugt¹,

Borne²,

Noord-Bokhorst³

et al. 1978

Vox Sanguinis

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The immunochemical characteristics of granulocyte alio- and autoantibodies can easily be studied with indirect immunofluorescence techniques. The correlation of these properties with the serological behavior of the antibodies and the clinical condition in which they were found was studied. The investigations included the determination of immunoglobulin class, subclass, light-chain composition, as well as optimal temperature of activity. Complement fixation in vitro was also investigated. Striking differences were found between IgG and IgM antibodies in their serological properties, especially in the granulocytotoxicity and leukoagglutination tests at different temperatures. Differences in light-chain and IgG subclass compositions of the antibodies did not seem to play a role. In studying the distribution of granulocyte-specific antigens on normal granulocytes and granulocytes in all stages of development, it was found that, while NAl5 NA2 and ND! are present in the same quantity on the cells of an individual, the NBt antigen is unequally distributed, both over ripe granulocytes and granulocyte precursors.

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The Heterogeneity of Erythrocyte Antigen Distribution in Human Normal Phenotypes: an Immunoelectron Microscopy Study

Cited by 21 publications

References 28 publications

Loss of red cell A, B, and H antigens is frequent in myeloid malignancies

Loss of red cell A, B, and H antigens is frequent in myeloid malignancies

Transfer of glycosylphosphatidylinositol-anchored proteins to deficient cells after erythrocyte transfusion in paroxysmal nocturnal hemoglobinuria

Serological, Immunochemical and Immuoncytological Properties of Granulocyte Antibodies

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