3D Analysis of CROMER (DAF) and a New Antigen CRAG

Overview

Journal Blood Transfus

Specialty Hematology

Date 2022 Feb 17

PMID 35175190

Authors

Aline Floch

Sunitha Vege

Kim Hue-Roye

Jan R Hamilton

Lance A Williams

Jacquelyn Choate

Christine Lomas-Francis

Connie M Westhoff

Affiliations

Soon will be listed here.

Abstract

Background: Cromer antigens are carried on decay accelerating factor (DAF, CD55), for which the crystal structure is available. We investigated two samples with an unidentified antibody to a high prevalence antigen and evaluate the location and characteristics of amino acids associated with antigens on the CD55 by 3D modelling.

Materials And Methods: Antigen typing and antibody identification were by standard methods. CD55 was sequenced, and Cromer variants were generated using the protein's crystal structure (1OK3, chain A). Antigen-associated residues and intraprotein interactions were investigated in 3D (Naccess, Protein Interactions Calculator).

Results: The antibody in the sample from a woman of Kashmiri descent was identified as anti-IFC (anti-CROM7). Her RBCs were negative for high-prevalence Cromer antigens including IFC. CD55 sequencing revealed a silent c.147G>A (p.Leu49=) and c.148G>T (p.Glu50Ter) changes, designated CROM*01N.05. The antibody in the sample from a woman of Greek ancestry was only compatible with IFC- RBCs but her RBCs were positive for known high-prevalence Cromer antigens. CD55 sequencing found she was homozygous for c.173A>G (p.Asp58Gly). The high prevalence antigen was named CRAG (ISBT CROM18 or 021018) and the allele designated CROM*01.-18. By 3D analysis, all known antigen-associated residues, including the new CRAG antigen, were exposed at the protein surface. Interactions between antigen-associated residues within the same CD55 domains were identified.

Discussion: Identification of antibodies to high prevalence Cromer antigens can be challenging. The surface exposure of antigen-associated residues likely accounts for their immunogenicity. 3D analysis of CD55 provides insight into previous serologic observations regarding the influence of some Cromer antigens on the expression of others.

Citing Articles

A structure-based analysis of the Kell blood group system.

Mayr G, Bublitz M, Steiert T, Loscher B, Wittig M, ElAbd H Front Immunol. 2024; 15:1452637.

PMID: 39726599 PMC: 11669894. DOI: 10.3389/fimmu.2024.1452637.

References

Storry J, Lomas-Francis C . The Cromer blood group system: an update. Immunohematology. 2021; 37(3):118-121. DOI: 10.21307/immunohematology-2021-017. View

Daniels G, Green C, Darr F, Anderson H, Sistonen P . A 'new' Cromer-related high frequency antigen probably antithetical to WES. Vox Sang. 1987; 53(4):235-8. DOI: 10.1111/j.1423-0410.1987.tb05073.x. View

Banks J, Poole J, Ahrens N, Seltsam A, Salama A, Hue-Roye K . SERF: a new antigen in the Cromer blood group system. Transfus Med. 2004; 14(4):313-8. DOI: 10.1111/j.0958-7578.2004.00519.x. View

Floch A, Pirenne F, Barrault A, Chami B, Toly-Ndour C, Tournamille C . Insights into anti-D formation in carriers of RhD variants through studies of 3D intraprotein interactions. Transfusion. 2021; 61(4):1286-1301. DOI: 10.1111/trf.16301. View

Daniels G, Green C, Powell R, Ward T . Hemagglutination inhibition of Cromer blood group antibodies with soluble recombinant decay-accelerating factor. Transfusion. 1998; 38(4):332-6. DOI: 10.1046/j.1537-2995.1998.38498257370.x. View

Holmes C, Simpson K, WAINWRIGHT S, Tate C, Houlihan J, Sawyer I . Preferential expression of the complement regulatory protein decay accelerating factor at the fetomaternal interface during human pregnancy. J Immunol. 1990; 144(8):3099-105. View

Lukacik P, Roversi P, White J, Esser D, Smith G, Billington J . Complement regulation at the molecular level: the structure of decay-accelerating factor. Proc Natl Acad Sci U S A. 2004; 101(5):1279-84. PMC: 337044. DOI: 10.1073/pnas.0307200101. View

Hue-Roye K, Lomas-Francis C, Belaygorod L, Lublin D, Barnes J, Chung A . Three new high-prevalence antigens in the Cromer blood group system. Transfusion. 2007; 47(9):1621-9. DOI: 10.1111/j.1537-2995.2007.01333.x. View

Vrignaud C, Chiaroni J, Durieux-Roussel E, Le Van Kim C, Azouzi S, Peyrard T . CORS (CROM20): A new high-prevalence antigen in the Cromer blood group system. Transfusion. 2020; 60(11):E40-E42. DOI: 10.1111/trf.16052. View

10.

Nakamura H . Roles of electrostatic interaction in proteins. Q Rev Biophys. 1996; 29(1):1-90. DOI: 10.1017/s0033583500005746. View

11.

Storry J, Sausais L, Hue-Roye K, Mudiwa F, Ferrer Z, Blajchman M . GUTI: a new antigen in the Cromer blood group system. Transfusion. 2003; 43(3):340-4. DOI: 10.1046/j.1537-2995.2003.00319.x. View

12.

Lublin D, Mallinson G, Poole J, Reid M, Thompson E, Ferdman B . Molecular basis of reduced or absent expression of decay-accelerating factor in Cromer blood group phenotypes. Blood. 1994; 84(4):1276-82. View

13.

Kowalski M, Pierce S, Edwards R, Ethirajan S, Ryan K, Livergood M . Hemolytic transfusion reaction due to anti-Tc(a). Transfusion. 1999; 39(9):948-50. DOI: 10.1046/j.1537-2995.1999.39090948.x. View

14.

Lublin D, Kompelli S, Storry J, Reid M . Molecular basis of Cromer blood group antigens. Transfusion. 2000; 40(2):208-13. DOI: 10.1046/j.1537-2995.2000.40020208.x. View

15.

Yazer M, Judd W, Davenport R, Dake L, Lomas-Francis C, Hue-Roye K . Case report and literature review: transient Inab phenotype and an agglutinating anti-IFC in a patient with a gastrointestinal problem. Transfusion. 2006; 46(9):1537-42. DOI: 10.1111/j.1537-2995.2006.00933.x. View

16.

Daniels G . Cromer-related antigens--blood group determinants on decay-accelerating factor. Vox Sang. 1989; 56(4):205-11. DOI: 10.1111/j.1423-0410.1989.tb02030.x. View

17.

Jallu V, Poulain P, Fuchs P, Kaplan C, de Brevern A . Modeling and molecular dynamics of HPA-1a and -1b polymorphisms: effects on the structure of the β3 subunit of the αIIbβ3 integrin. PLoS One. 2012; 7(11):e47304. PMC: 3498292. DOI: 10.1371/journal.pone.0047304. View

18.

Telen M, Hall S, Green A, Moulds J, Rosse W . Identification of human erythrocyte blood group antigens on decay-accelerating factor (DAF) and an erythrocyte phenotype negative for DAF. J Exp Med. 1988; 167(6):1993-8. PMC: 2189670. DOI: 10.1084/jem.167.6.1993. View

19.

Dho S, Lim J, Kim L . Beyond the Role of CD55 as a Complement Component. Immune Netw. 2018; 18(1):e11. PMC: 5833118. DOI: 10.4110/in.2018.18.e11. View

20.

Bartels C, Zelinski T, Lockridge O . Mutation at codon 322 in the human acetylcholinesterase (ACHE) gene accounts for YT blood group polymorphism. Am J Hum Genet. 1993; 52(5):928-36. PMC: 1682033. View