The Gerbich blood group system: old knowledge, new importance

Jaśkiewicz, Ewa; Peyrard, Thierry; Kaczmarek, Radosław; Zerka, Agata; Jodłowska, Marlena; Czerwiński, Marcin

doi:10.1016/j.tmrv.2018.02.004

Cited by 19 publications

(20 citation statements)

References 94 publications

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“…The Ge blood group antigens are expressed on glycophorin C (GPC) and glycoprotein D (GPD); the former is expressed on very early erythroid progenitor cells, as shown in Table 1 [8,15]. GPC, in a ternary complex with protein 4 and p55, exists abundantly at 2.0 × 10 5 copies per cell, 90 % of which are integrated in the cytoskeleton and deemed essential for maintaining red cell shape and membrane functions [16].…”

Section: Anti-gerbich (Ge)-mediated Adfn (Fig 3)mentioning

confidence: 99%

Three non-classical mechanisms for anemic disease of the fetus and newborn, based on maternal anti-Kell, anti-Ge3, anti-M, and anti-Jra cases

Ohto

Denomme

et al. 2020

Transfusion and Apheresis Science

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Maternal alloantibody-mediated hemolytic disease of the fetus and newborn (HDFN) ranges from no or mild symptoms to severe hydrops and intrauterine fetal demise. Hemolytic anti-D-mediated HDFN proceeds via a longknown mechanism, to which three other pathways to fetal/neonatal anemia may be added: (0) Fetal erythrocyte destruction can proceed by extravascular phagocytosis. (1) An apoptotic pathway has been described for anti-Kell, and anti-Ge3. (2) Erythropoietic suppression may arise from altered or deformed erythroblast architecture in anti-M-mediated disease. (3) Clonal escape from erythropoietic suppression is hypothesized to arise from maternal anti-Jr a immune pressure, albeit this requires further elucidation. Alloantibody-mediated anemic disease of the fetus and newborn (ADFN) is a designation we favor for cases when hemolysis or hyperbilirubinemia are not the dominant features, such as those provoked by anti-Kell, anti-Ge3, anti-M, and anti-Jr a .

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Section: Anti-gerbich (Ge)-mediated Adfn (Fig 3)mentioning

confidence: 99%

Three non-classical mechanisms for anemic disease of the fetus and newborn, based on maternal anti-Kell, anti-Ge3, anti-M, and anti-Jra cases

Ohto

Denomme

et al. 2020

Transfusion and Apheresis Science

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“…Amino acid sequence of external (aa 1–40) domain of GPB, its glycan structure and attachment sites [1, 4 modified]…”

Section: Introductionmentioning

confidence: 99%

“…However, RBCs lacking GPA [En(a-)], GPB (S-s-U-), or GPA and GPB [Dombrock, Gy(a-b-)] proved to bind EBA-140 effectively. Other RBC variants of the Yus and Gerbich phenotype, encoded by the genes lacking exons 2 or 3 in the GYPC gene [4] resulting in deletion of GPC amino acid residues 17–35 and 36–63, respectively, showed markedly reduced binding [75]. Moreover, only RBCs of the Leach phenotype (GPC null), lacking GPC, were not bound by EBA-140 ligand.…”

Section: Introductionmentioning

confidence: 99%

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Erythrocyte glycophorins as receptors for Plasmodium merozoites

et al. 2019

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Glycophorins are heavily glycosylated sialoglycoproteins of human and animal erythrocytes. In humans, there are four glycophorins: A, B, C and D. Glycophorins play an important role in the invasion of red blood cells (RBCs) by malaria parasites, which involves several ligands binding to RBC receptors. Four Plasmodium falciparum merozoite EBL ligands have been identified: erythrocyte-binding antigen-175 (EBA-175), erythrocyte-binding antigen-181 (EBA-181), erythrocyte-binding ligand-1 (EBL-1) and erythrocyte-binding antigen-140 (EBA-140). It is generally accepted that glycophorin A (GPA) is the receptor for P. falciparum EBA-175 ligand. It has been shown that α(2,3) sialic acid residues of GPA O-glycans form conformation-dependent clusters on GPA polypeptide chain which facilitate binding. P. falciparum can also invade erythrocytes using glycophorin B (GPB), which is structurally similar to GPA. It has been shown that P. falciparum EBL-1 ligand binds to GPB. Interestingly, a hybrid GPB-GPA molecule called Dantu is associated with a reduced risk of severe malaria and ameliorates malaria-related morbidity. Glycophorin C (GPC) is a receptor for P. falciparum EBA-140 ligand. Likewise, successful binding of EBA-140 depends on sialic acid residues of N- and O-linked oligosaccharides of GPC, which form a cluster or a conformational structure depending on the presence of peptide fragment encompassing amino acids (aa) 36–63. Evaluation of the homologous P. reichenowi EBA-140 unexpectedly revealed that the chimpanzee homolog of human glycophorin D (GPD) is probably the receptor for this ligand. In this review, we concentrate on the role of glycophorins as erythrocyte receptors for Plasmodium parasites. The presented data support the long-lasting idea of high evolutionary pressure exerted by Plasmodium on the human glycophorins, which emerge as important receptors for these parasites.

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“…1 There are six known high-prevalence antigens (Ge2, Ge3, Ge4, GEPL, GEAT, and GETI) and five low-prevalence antigens (Wb, Ls a , An a , Dh a , and GEIS). 2 In Melanesians of Papua New Guinea, over 50% of the population is Ge-negative, and about 10% is reported to have natural anti-Ge. 3 In general, however, Ge is a very common blood group system; therefore, it is considered to be extremely difficult to find compatible blood components for patients with anti-Ge.…”

Section: Introductionmentioning

confidence: 99%

Identification of Anti-Gerbich Antibody in an Emirati Marrow Hematopoietic Progenitor Cell Donor with Fy(a−b−) Phenotype

et al. 2018

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In this study, we report a case of anti-Gerbich (Ge) alloantibody to a high-prevalence Ge antigen in a donor with Fy(a−b−) phenotype. The alloantibody was detected in an Emirati boy who was admitted to a Korean tertiary hospital for marrow hematopoietic progenitor cell donation. He did not have a history of transfusion. His blood type was A, RhD+, and findings from the antibody screening and identification test showed 2+ reactivity in all panel cells except autologous cells. We concluded that it would be very difficult to find compatible blood components for the donor and requested further tests from external laboratories. Anti-Ge2 was identified by additional tests in a foreign reference laboratory, and the Duffy genotype of the donor was FY*02/FY*02N.01 based on the Korean Rare Blood Program. Although the donor was not a Korean, as the number of foreign patients visiting Korea increases annually, there is growing interest in patients with rare blood types in the Korean population. However, there has been very little research on rare or high prevalence blood type antigen and antibody in the Korean population. Therefore, additional research in Korea is needed on rare blood group antibodies and antigens, including Ge cases.

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The Gerbich blood group system: old knowledge, new importance

Cited by 19 publications

References 94 publications

Three non-classical mechanisms for anemic disease of the fetus and newborn, based on maternal anti-Kell, anti-Ge3, anti-M, and anti-Jra cases

Three non-classical mechanisms for anemic disease of the fetus and newborn, based on maternal anti-Kell, anti-Ge3, anti-M, and anti-Jra cases

Erythrocyte glycophorins as receptors for Plasmodium merozoites

Identification of Anti-Gerbich Antibody in an Emirati Marrow Hematopoietic Progenitor Cell Donor with Fy(a−b−) Phenotype

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