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Ree IMC, Besuden CFJ, Wintjens V, et al. Exchange transfusions in severe Rh-mediated alloimmune haemolytic disease of the foetus and newborn: a 20-year overview on the incidence, associated risks and outcome. Vox Sang 2021;116:990–7.ReeIMCBesudenCFJWintjensVet alExchange transfusions in severe Rh-mediated alloimmune haemolytic disease of the foetus and newborn: a 20-year overview on the incidence, associated risks and outcome2021116990710.1111/vox.13090859639433730387Search in Google Scholar
Floch A. Maternal Red Blood Cell Alloimmunisation Working Party, literature review. RH blood group system: rare specificities. Transfus Clin Biol 2021;28:314–20.FlochAMaternal Red Blood Cell Alloimmunisation Working Party, literature review2021283142010.1016/j.tracli.2021.04.00733895380Search in Google Scholar
Pegoraro V, Urbinati D, Visser GHA, et al. Hemolytic disease of the fetus and newborn due to Rh(D) incompatibility: a preventable disease that still produces significant morbidity and mortality in children. PLoS One 2020;15:e0235807.PegoraroVUrbinatiDVisserGHAet alHemolytic disease of the fetus and newborn due to Rh(D) incompatibility: a preventable disease that still produces significant morbidity and mortality in children202015e023580710.1371/journal.pone.0235807737120532687543Search in Google Scholar
Gudlaugsson B, Hjartardottir H, Svansdottir G, et al. Rhesus D alloimmunization in pregnancy from 1996 to 2015 in Iceland: a nation-wide population study prior to routine antenatal anti-D prophylaxis. Transfusion 2020;60:175–83.GudlaugssonBHjartardottirHSvansdottirGet alRhesus D alloimmunization in pregnancy from 1996 to 2015 in Iceland: a nation-wide population study prior to routine antenatal anti-D prophylaxis2020601758310.1111/trf.1563531850521Search in Google Scholar
Dajak S, Stefanović V, Capkun V. Severe hemolytic disease of fetus and newborn caused by red blood cell antibodies undetected at first–trimester screening (CME). Transfusion 2011;51:1380–8.DajakSStefanovićVCapkunVSevere hemolytic disease of fetus and newborn caused by red blood cell antibodies undetected at first–trimester screening (CME)2011511380810.1111/j.1537-2995.2010.03006.x21214583Search in Google Scholar
Turley E, McGowan EC, Hyland CA, et al. Severe hemolytic disease of the fetus and newborn due to allo-anti-D in a patient with a partial DEL phenotype arising from the variant allele described as RHD*148+1T (RHD*01EL.31). Transfusion 2018;58:2260–4.TurleyEMcGowanECHylandCAet alSevere hemolytic disease of the fetus and newborn due to allo-anti-D in a patient with a partial DEL phenotype arising from the variant allele described as RHD*148+1T (RHD*01EL.31)2018582260410.1111/trf.1494430222865Search in Google Scholar
Bub CB, Aravechia MG, Costa TH, Kutner JM, Castilho L. RHD alleles among pregnant women with serologic discrepant weak D phenotypes from a multiethnic population and risk of alloimmunization. J Clin Lab Anal 2018;32:e22221.BubCBAravechiaMGCostaTHKutnerJMCastilhoLRHD alleles among pregnant women with serologic discrepant weak D phenotypes from a multiethnic population and risk of alloimmunization201832e2222110.1002/jcla.22221681698328374955Search in Google Scholar
Lukacevic Krstic J, Dajak S, Bingulac-Popovic J, Dogic V, Mratinovic-Mikulandra J. Anti-D reagents should be chosen accordingly to the prevalence of D variants in the obstetric population. J Clin Lab Anal 2018;32:e22285.LukacevicKrstic JDajakSBingulac-PopovicJDogicVMratinovic-MikulandraJAnti-D reagents should be chosen accordingly to the prevalence of D variants in the obstetric population201832e2228510.1002/jcla.22285681708828649781Search in Google Scholar
Quantock KM, Lopez GH, Hyland CA, et al. Anti-D in a mother, hemizygous for the variant RHD*DNB gene, associated with hemolytic disease of the fetus and newborn. Transfusion 2017;57:1938–43.QuantockKMLopezGHHylandCAet alAnti-D in a mother, hemizygous for the variant RHD*DNB gene, associated with hemolytic disease of the fetus and newborn20175719384310.1111/trf.1415628639307Search in Google Scholar
Duncan JA, Nahirniak S, Onell R, Clarke G. Two cases of the variant RHD*DAU5 allele associated with maternal alloanti-D. Immunohematology 2017;33:60–3.DuncanJANahirniakSOnellRClarkeGTwo cases of the variant RHD*DAU5 allele associated with maternal alloanti-D20173360310.21307/immunohematology-2019-009Search in Google Scholar
Lukacevic Krstic J, Dajak S, Bingulac-Popovic J, Dogic V, Mratinovic-Mikulandra J. Anti-D antibodies in pregnant D variant antigen carriers initially typed as RhD. Transfus Med Hemother 2016;43:419–24.LukacevicKrstic JDajakSBingulac-PopovicJDogicVMratinovic-MikulandraJAnti-D antibodies in pregnant D variant antigen carriers initially typed as RhD2016434192410.1159/000446816515971227994529Search in Google Scholar
Sandler SG, Flegel WA, Westhoff CM, et al. It’s time to phase in RHD genotyping for patients with a serologic weak D phenotype: College of American Pathologists Transfusion Medicine Resource Committee Work Group. Transfusion 2015;55:680–9.SandlerSGFlegelWAWesthoffCMet alIt’s time to phase in RHD genotyping for patients with a serologic weak D phenotype: College of American Pathologists Transfusion Medicine Resource Committee Work Group201555680910.1111/trf.12941435754025438646Search in Google Scholar
Flegel WA, Denomme GA, Queenan JT, et al. It’s time to phase out “serologic weak D phenotype” and resolve D types with RHD genotyping including weak D type 4. Transfusion 2020;60:855–9.FlegelWADenommeGAQueenanJTet alIt’s time to phase out “serologic weak D phenotype” and resolve D types with RHD genotyping including weak D type 4202060855910.1111/trf.15741912135032163599Search in Google Scholar
Sandler SG, Chen LN, Flegel WA. Serological weak D phenotypes: a review and guidance for interpreting the RhD blood type using the RHD genotype. Br J Haematol 2017;179:10–9.SandlerSGChenLNFlegelWASerological weak D phenotypes: a review and guidance for interpreting the RhD blood type using the RHD genotype201717910910.1111/bjh.14757561284728508413Search in Google Scholar
Wagner FF, Flegel WA. The Rhesus Site. Transfus Med Hemother 2014;41:357–63.WagnerFFFlegelWAThe Rhesus Site2014413576310.1159/000366176426449225538538Search in Google Scholar
Storry JR, Clausen FB, Castilho L, et al. International Society of Blood Transfusion Working Party on Red Cell Immunogenetics and Blood Group Terminology: Report of the Dubai, Copenhagen and Toronto meetings. Vox Sang 2019;114:95–102.StorryJRClausenFBCastilhoLet alInternational Society of Blood Transfusion Working Party on Red Cell Immunogenetics and Blood Group Terminology: Report of the Dubai, Copenhagen and Toronto meetings20191149510210.1111/vox.12717634265230421425Search in Google Scholar
Flegel WA. Proceed with care: the “uncommon” serologic weak D phenotypes. Blood Transfus 2021;19:272–6.FlegelWAProceed with care: the “uncommon” serologic weak D phenotypes2021192726Search in Google Scholar
International Society of Blood Transfusion. Names for RHD (ISBT 004) Blood Group Alleles (ISBT_004__RHD_blood_ group_alleles_v6.0_30–NOV–2021.pdf). https://www. isbtweb.org/resource/004rhd.html. Accessed 2 February 2022.International Society of Blood Transfusionhttps://www. isbtweb.org/resource/004rhd.htmlAccessed 2 February2022Search in Google Scholar
Wagner FF, Frohmajer A, Ladewig B, et al. Weak D alleles express distinct phenotypes. Blood 2000;95:2699–708.WagnerFFFrohmajerALadewigBet alWeak D alleles express distinct phenotypes200095269970810.1182/blood.V95.8.2699Search in Google Scholar
Wagner FF, Ladewig B, Angert KS, Heymann GA, Eicher NI, Flegel WA. The DAU allele cluster of the RHD gene. Blood 2002;100:306–11.WagnerFFLadewigBAngertKSHeymannGAEicherNIFlegelWAThe DAU allele cluster of the RHD gene20021003061110.1182/blood-2002-01-032012070041Search in Google Scholar
Flegel WA, von Zabern I, Doescher A, et al. D variants at the RhD vestibule in the weak D type 4 and Eurasian D clusters. Transfusion 2009;49:1059–69.FlegelWAvon ZabernIDoescherAet alD variants at the RhD vestibule in the weak D type 4 and Eurasian D clusters20094910596910.1111/j.1537-2995.2009.02102.x19309476Search in Google Scholar
Hemker MB, Ligthart PC, Berger L, van Rhenen DJ, van der Schoot CE, Wijk PA. DAR, a new RhD variant involving exons 4, 5, and 7, often in linkage with ceAR, a new Rhce variant frequently found in African blacks. Blood 1999;94:4337–42.HemkerMBLigthartPCBergerLvanRhenen DJvander Schoot CEWijkPADAR, a new RhD variant involving exons 4, 5, and 7, often in linkage with ceAR, a new Rhce variant frequently found in African blacks19999443374210.1182/blood.V94.12.4337Search in Google Scholar
Yu X, Wagner FF, Witter B, Flegel WA. Outliers in RhD membrane integration are explained by variant RH haplotypes. Transfusion 2006;46:1343–51.YuXWagnerFFWitterBFlegelWAOutliers in RhD membrane integration are explained by variant RH haplotypes20064613435110.1111/j.1537-2995.2006.00902.x16934070Search in Google Scholar
Horuk R, Martin AW, Wang Z, et al. Expression of chemokine receptors by subsets of neurons in the central nervous system. J Immunol 1997;158:2882–90.HorukRMartinAWWangZet alExpression of chemokine receptors by subsets of neurons in the central nervous system199715828829010.4049/jimmunol.158.6.2882Search in Google Scholar
Huh JY, Park G, Jang SJ, Moon DS, Park YJ. A rapid long PCR-direct sequencing analysis for ABO genotyping. Ann Clin Lab Sci 2011;41:340–5.HuhJYParkGJangSJMoonDSParkYJA rapid long PCR-direct sequencing analysis for ABO genotyping2011413405Search in Google Scholar
Wagner FF, Gassner C, Müller TH, Schönitzer D, Schunter F, Flegel WA. Molecular basis of weak D phenotypes. Blood 1999;93:385–93.WagnerFFGassnerCMüllerTHSchönitzerDSchunterFFlegelWAMolecular basis of weak D phenotypes1999933859310.1182/blood.V93.1.385Search in Google Scholar
Fasano RM, Monaco A, Meier ER, et al. RH genotyping in a sickle cell disease patient contributing to hematopoietic stem cell transplantation donor selection and management. Blood 2010;116:2836–8.FasanoRMMonacoAMeierERet alRH genotyping in a sickle cell disease patient contributing to hematopoietic stem cell transplantation donor selection and management20101162836810.1182/blood-2010-04-279372297459120644109Search in Google Scholar
Ouchari M, Srivastava K, Döscher A, et al. Serologic and molecular characterization of weak D type 29. Transfusion 2017;57:2542–4.OuchariMSrivastavaKDöscherAet alSerologic and molecular characterization of weak D type 292017572542410.1111/trf.14218561284928671325Search in Google Scholar
Wagner FF, Flegel WA. RHD gene deletion occurred in the Rhesus box. Blood 2000;95:3662–8.WagnerFFFlegelWARHD gene deletion occurred in the Rhesus box2000953662810.1182/blood.V95.12.3662Search in Google Scholar
Srivastava K, Polin H, Sheldon SL, et al. The DAU cluster: a comparative analysis of 18 RHD alleles, some forming partial D antigens. Transfusion 2016;56:2520–31.SrivastavaKPolinHSheldonSLet alThe DAU cluster: a comparative analysis of 18 RHD alleles, some forming partial D antigens20165625203110.1111/trf.13739549951727480171Search in Google Scholar
Flegel WA, Gassner C, Muller TH, Schonitzer D, Schunter F, Wagner FF. The molecular basis of weak D (abstract). Vox Sang 1998;74:15.FlegelWAGassnerCMullerTHSchonitzerDSchunterFWagnerFFThe molecular basis of weak D (abstract)19987415Search in Google Scholar
Wagner FF, Frohmajer A, Flegel WA. RHD positive haplotypes in D negative Europeans. BMC Genet 2001;2:10.WagnerFFFrohmajerAFlegelWARHD positive haplotypes in D negative Europeans200121010.1186/1471-2156-2-103726711495631Search in Google Scholar
Wolinsky H. A mythical beast: increased attention highlights the hidden wonders of chimeras. EMBO Rep 2007;8:212–4.WolinskyHA mythical beast: increased attention highlights the hidden wonders of chimeras20078212410.1038/sj.embor.7400918180803917330063Search in Google Scholar
Körmöczi GF, Dauber EM, Haas OA, et al. Mosaicism due to myeloid lineage restricted loss of heterozygosity as cause of spontaneous Rh phenotype splitting. Blood 2007;110: 2148–57.KörmöcziGFDauberEMHaasOAet alMosaicism due to myeloid lineage restricted loss of heterozygosity as cause of spontaneous Rh phenotype splitting200711021485710.1182/blood-2007-01-06810617537994Search in Google Scholar
Dauber EM, Mayr WR, Hustinx H, et al. Somatic mosaicisms of chromosome 1 at two different stages of ontogenetic development detected by Rh blood group discrepancies. Haematologica 2019;104:632–8.DauberEMMayrWRHustinxHet alSomatic mosaicisms of chromosome 1 at two different stages of ontogenetic development detected by Rh blood group discrepancies2019104632810.3324/haematol.2018.201293639533830237270Search in Google Scholar
Lin JJ, Wang XD, Zhu SY. α-1,3-N-acetylgalactose aminotransferase gene 539G>C mutation leads to the A2B isoform. Genet Mol Res 2014;13:2987–93.LinJJWangXDZhuSYα-1,3-N-acetylgalactose aminotransferase gene 539G>C mutation leads to the A2B isoform20141329879310.4238/2014.April.16.724782133Search in Google Scholar
Reiss RF, Malavade V, Johnson CL, Hendricks E, Rabin BI, Marsh WL. Blood grouping with the Olympus PK7100 testing system. Clin Lab Haematol 1988;10:385–90.ReissRFMalavadeVJohnsonCLHendricksERabinBIMarshWLBlood grouping with the Olympus PK7100 testing system1988103859010.1111/j.1365-2257.1988.tb01185.x3150697Search in Google Scholar
Saboor M, Zehra A, Hamali HA, et al. Prevalence of A(2) and A(2)B subgroups and anti–A(1) antibody in blood donors in Jazan, Saudi Arabia. Int J Gen Med 2020;13:787–90.SaboorMZehraAHamaliHAet alPrevalence of A(2) and A(2)B subgroups and anti–A(1) antibody in blood donors in Jazan, Saudi Arabia2020137879010.2147/IJGM.S272698754823733116770Search in Google Scholar
Klein HG, Anstee DJ, Eds. ABO, H, LE, P1PK, GLOB, I and FORS blood group systems. In: Mollison’s blood transfusion in clinical medicine. 12th ed. Oxford: Blackwell Publishing Ltd., 2014:121.KleinHGAnsteeDJEdsOxfordBlackwell Publishing Ltd201412110.1002/9781118689943Search in Google Scholar
International Society of Blood Transfusion. Names for ABO (ISBT 001) Blood Group Alleles (001_ABO_Alleles_v1.2.pdf). https://www.isbtweb.org/resource/001aboalleles.html. Accessed 2 February 2022.International Society of Blood Transfusionhttps://www.isbtweb.org/resource/001aboalleles.htmlAccessed 2 February2022Search in Google Scholar
Reyes F, Gourdin MF, Lejonc JL, Cartron JP, Gorius JB, Dreyfus B. The heterogeneity of erythrocyte antigen distribution in human normal phenotypes: an immunoelectron microscopy study. Br J Haematol 1976;34:613–21.ReyesFGourdinMFLejoncJLCartronJPGoriusJBDreyfusBThe heterogeneity of erythrocyte antigen distribution in human normal phenotypes: an immunoelectron microscopy study1976346132110.1111/j.1365-2141.1976.tb03608.x791344Search in Google Scholar
Dogic V, Bingulac-Popovic J, Babic I, et al. Distribution of weak D types in the Croatian population. Transfus Med 2011;21:278–9.DogicVBingulac-PopovicJBabicIet alDistribution of weak D types in the Croatian population201121278910.1111/j.1365-3148.2011.01071.x21269342Search in Google Scholar
Flegel WA, Wagner FF, Ó Donghaile DP. Anti-D immunization rates may exceed 50% in many clinically relevant settings, despite varying widely among patient cohorts. Transfusion 2020;60:1109–10.FlegelWAWagnerFFÓDonghaile DPAnti-D immunization rates may exceed 50% in many clinically relevant settings, despite varying widely among patient cohorts20206011091010.1111/trf.15788906734932421874Search in Google Scholar
Flegel WA. Molecular genetics and clinical applications for RH. Transfus Apher Sci 2011;44:81–91.FlegelWAMolecular genetics and clinical applications for RH201144819110.1016/j.transci.2010.12.013304251121277262Search in Google Scholar
Cornish VW, Kaplan MI, Veenstra DL, Kollman PA, Schultz PG. Stabilizing and destabilizing effects of placing beta-branched amino acids in protein alpha-helices. Biochemistry 1994;33:12022–31.CornishVWKaplanMIVeenstraDLKollmanPASchultzPGStabilizing and destabilizing effects of placing beta-branched amino acids in protein alpha-helices199433120223110.1021/bi00206a0037918421Search in Google Scholar
Bruce LJ, Ghosh S, King MJ, et al. Absence of CD47 in protein 4.2-deficient hereditary spherocytosis in man: an interaction between the Rh complex and the band 3 complex. Blood 2002;100:1878–85.BruceLJGhoshSKingMJet alAbsence of CD47 in protein 4.2-deficient hereditary spherocytosis in man: an interaction between the Rh complex and the band 3 complex200210018788510.1182/blood-2002-03-070612176912Search in Google Scholar
Dahl KN, Parthasarathy R, Westhoff CM, Layton DM, Discher DE. Protein 4.2 is critical to CD47-membrane skeleton attachment in human red cells. Blood 2004;103:1131–6.DahlKNParthasarathyRWesthoffCMLaytonDMDischerDEProtein 4.2 is critical to CD47-membrane skeleton attachment in human red cells20041031131610.1182/blood-2003-04-133114551146Search in Google Scholar
Nicolas V, Le Van Kim C, Gane P, et al. Rh-RhAG/ankyrin-R, a new interaction site between the membrane bilayer and the red cell skeleton, is impaired by Rh(null)-associated mutation. J Biol Chem 2003;278:25526–33.NicolasVLe VanKim CGanePet alRh-RhAG/ankyrin-R, a new interaction site between the membrane bilayer and the red cell skeleton, is impaired by Rh(null)-associated mutation2003278255263310.1074/jbc.M30281620012719424Search in Google Scholar
Luettringhaus TA, Cho D, Ryang DW, Flegel WA. An easy RHD genotyping strategy for D– East Asian persons applied to Korean blood donors. Transfusion 2006;46:2128–37.LuettringhausTAChoDRyangDWFlegelWAAn easy RHD genotyping strategy for D– East Asian persons applied to Korean blood donors20064621283710.1111/j.1537-2995.2006.01042.x17176325Search in Google Scholar
Denomme GA, Dake LR, Vilensky D, Ramyar L, Judd WJ. Rh discrepancies caused by variable reactivity of partial and weak D types with different serologic techniques. Transfusion 2008;48:473–8.DenommeGADakeLRVilenskyDRamyarLJuddWJRh discrepancies caused by variable reactivity of partial and weak D types with different serologic techniques200848473810.1111/j.1537-2995.2007.01551.x18067505Search in Google Scholar
Tammi SM, Tounsi WA, Sainio S, et al. Next-generation sequencing of 35 RHD variants in 16 253 serologically D– pregnant women in the Finnish population. Blood Adv 2020;4:4994–5001.TammiSMTounsiWASainioSet alNext-generation sequencing of 35 RHD variants in 16 253 serologically D– pregnant women in the Finnish population202044994500110.1182/bloodadvances.2020001569759440333057632Search in Google Scholar
de Moura Neto JP, Cerqueira BAV, Santos WVB, Lyra IM, Goncalves MS. The DAU allele and anti-D alloimmunization present with high frequency in Brazilian sickle cell disease patients. J Hematol 2017;6:73–80.deMoura Neto JPCerqueiraBAVSantosWVBLyraIMGoncalvesMSThe DAU allele and anti-D alloimmunization present with high frequency in Brazilian sickle cell disease patients20176738010.14740/jh316w715584732300397Search in Google Scholar
Karnot A, Woestmann SJ, Flesch BK. Weak RhD phenotype caused by compound heterozygosity for DAU-2 and a new RHD*c393-394 dupGG-mutation (abstract). Transfus Med Hemother 2016;43:42–3.KarnotAWoestmannSJFleschBKWeak RhD phenotype caused by compound heterozygosity for DAU-2 and a new RHD*c393-394 dupGG-mutation (abstract)201643423Search in Google Scholar
Wagner FF, Moulds JM, Tounkara A, Kouriba B, Flegel WA. RHD allele distribution in Africans of Mali. BMC Genet 2003;4:14.WagnerFFMouldsJMTounkaraAKouribaBFlegelWARHD allele distribution in Africans of Mali200341410.1186/1471-2156-4-1422291214505497Search in Google Scholar
Kulkarni SS, Gogri H, Parchure D, et al. RHD–positive alleles among D– C/E+ individuals from India. Transfus Med Hemother 2018;45:173–7.KulkarniSSGogriHParchureDet alRHD–positive alleles among D– C/E+ individuals from India201845173710.1159/000479239600660029928172Search in Google Scholar
Fichou Y, Le Maréchal C, Bryckaert L, et al. A convenient qualitative and quantitative method to investigate RHD-RHCE hybrid genes. Transfusion 2013;53:2974–82.FichouYLe MaréchalCBryckaertLet alA convenient qualitative and quantitative method to investigate RHD-RHCE hybrid genes201353297482Search in Google Scholar
Heilig EA, Gutti U, Tai T, Shen J, Kelleher RJ 3rd. Trans-dominant negative effects of pathogenic PSEN1 mutations on γ-secretase activity and Aβ production. J Neurosci 2013;33:11606–17.HeiligEAGuttiUTaiTShenJKelleherRJ3rdTrans-dominant negative effects of pathogenic PSEN1 mutations on γ-secretase activity and Aβ production201333116061710.1523/JNEUROSCI.0954-13.2013372454923843529Search in Google Scholar