Produção Nacional
Revisado por pares
International Society of Blood Transfusion Committee on Terminology for Red Blood Cell Surface Antigens: Macao report
2008; Wiley; Volume: 96; Issue: 2 Linguagem: Inglês
10.1111/j.1423-0410.2008.01133.x
ISSN1423-0410
AutoresGeoff Daniels, Lilian Castilho, Willy A. Flegel, Anne Fletcher, George Garratty, C. Levene, Christine Lomas‐Francis, J.M. Moulds, J. J. Moulds, Martin L. Olsson, M.A.M. Overbeeke, Joyce Poole, Marion E. Reid, P. Rouger, C. Ellen van der Schoot, Marion L. Scott, P. Sistonen, E. Smart, J. R. Storry, Yoshihiko Tani, L.‐C. Yu, Silvano Wendel, Connie M. Westhoff, Vered Yahalom, Teresa Zelinski,
Tópico(s)Blood disorders and treatments
ResumoThe committee met in Macao Special Administrative Region, China, during the 2008 International Society of Blood Transfusion (ISBT) Congress. Some changes to the classification documented in Blood Group Terminology 2004 [1] and updated in 2007 [2] were agreed and are described below. The full updated classification can be found on the blood group terminology website at http://www.blood.co.uk/ibgrl. A new blood group system, the RHAG system, was established and new antigens were added to the Rh, Kell, and Dombrock systems (Table 1). A total of 308 antigens are now recognized, 270 of which are clustered in 30 blood group systems. One high-incidence antigen has been added to the Rh system. RH57 (CEST) is antithetical to the low-incidence antigen RH48 (JAL) and is defined by an antibody produced by an RH:48,–57 patient who is homozygous for an RHCE allele encoding RH48 and an Arg114Trp substitution in the RhCcEe protein [3] (Table 1). Three antigens of high incidence were added to the Kell system: KEL32 (KUCI), KEL33 (KANT) and KEL34 (KASH). Antibodies defining these antigens were non-reactive with KO (Kell-null) red blood cells. The KEL:–32 proposita and her KEL:–32 sister are heterozygous for a KEL allele encoding Ala424Val. No cause for the apparent silencing of the KEL gene in trans was found [4]. Anti-KEL33 was produced in an individual heterozygous for a KEL allele encoding Arg428Leu and for a known KEL*0 allele [4]. KEL:–32 red blood cells are also KEL:–33, but KEL:–33 cells are KEL:32. The antibody defining KEL34 (KASH) is non-reactive with the red blood cells of the antibody maker and with those of her sister. Both the KEL:–34 propositus and her KEL:–34 sister have a Kmod phenotype and are homozygous for a KEL allele encoding a Tyr253Cys substitution (Poole J, Karamatic Crew, V, unpublished observations). DO6 (DOYA) is defined by an antibody to a high-incidence antigen produced in a patient who was homozygous for DO*1 (793A) and for a novel DO mutation encoding Tyr183Asp (Table 1). The red blood cells of the antibody maker are DO:–1,–2 with weakened expression of DO3, DO4, and DO5. Anti-DO6 reacts with red blood cells of common Dombrock type, but weakly with DO:−4 (Hy−) and DO:−5 [Jo(a−)] red blood cells, and is non-reactive with DO:−3 [Gy(a−)] cells [5]. RHAG is a new blood group system comprising three antigens, one of which is assigned provisionally. Antigens of this system appear to be located on the Rh-associated glycoprotein (CD241) encoded by the RHAG gene [6]. RHAG1 (Duclos) was previously the high-incidence antigen 901013. The antibody defining RHAG1 (Duclos) reacts with all red blood cells apart from those of the antibody maker and those Rhnull red blood cells that lack MNS5 (U) [7]. The antibody maker, whose red blood cells had normal Rh antigens and slightly weakened MNS5 [8], was homozygous for 316C>G in RHAG encoding Gln106Glu (Table 1). HEK293 cells expressing normal RHAG reacted with anti-RHAG1, whereas those expressing RHAG containing 316C>G did not [8]. RHAG2 (Ola) was previously the low-incidence antigen 700043. The original family study showed that RHAG2 expression is associated with weakened expression of Rh antigens, but that the gene governing RHAG2 is not located at the Rh locus [9]. Two RHAG:2 members of the original family are heterozygous for a nucleotide change in RHAG encoding Ser227Leu close to the fourth predicted loop of the Rh-associated glycoprotein [8]. In addition, red blood cells of a Japanese individual with the Rhmod phenotype and homozygous for the Ser227Leu mutation [10] were subsequently shown to be Ol(a+) (Tilley L, Poole J, Daniels G, unpublished observations). RHAG3 (DSLK) is a high-incidence antigen defined by an antibody with reactivity characteristics similar to those of anti-RHAG1 (non-reactive with Rhnull MNS:−5 cells, reactive with Rhnull MNS:5 cells), but the red blood cells of the RHAG:−3 antibody maker were RHAG:1. This RHAG:−3 patient was homozygous for a mutation in RHAG encoding Lys164Gln [8]. Owing to incomplete evidence, RHAG3 is provisionally assigned to the RHAG system. DSLK was initially named DL [8], but changed to DSLK (from letters in 'Duclos-like') to comply with the rule that symbols for designating new specificities will consist of three to six on-line, capital letters [1]. 700043 (Ola) has been assigned RHAG2 and is now obsolete. 901013 (Duclos) has been assigned RHAG1 and is now obsolete. Many of the traditional symbols for blood group antigens and phenotypes incorporate superscripts and subscripts. In circumstances where superscripts and subscripts are not available, the superscript or subscript should be written on the line. For example, Jka would be Jka. Work is continuing on the establishment of a terminology for blood group alleles and on the development of a new collection containing antigens on glycophorin A that are determined primarily by glycosylation, including Hu, M1, Tm, Sj and Can. Dr Cyril Levene has retired from the committee. We would like to thank him for his contributions over many years. Dr GL Daniels (Chair): Bristol Institute for Transfusion Sciences, NHS Blood and Transplant, Filton, Bristol, UK. geoff.daniels@nbs.nhs.uk Prof Dr L. Castilho: University of Campinas/Hemocentro, Campinas, Brazil. castilho@unicamp.br Prof WA Flegel: University Hospital, Ulm, Germany. willy.flegel@uni-ulm.de Prof G Garratty: American Red Cross Blood Services, Southern California Region, Pomona, CA, USA. garratty@usa.redcross.org Ms C Lomas-Francis: New York Blood Center, New York, NY, USA. clomas-francis@nybloodcentre.org Mr JJ Moulds: LifeShare Blood Centers, Shreveport, LA, USA. jjmoulds@lifeshare.org Dr JM Moulds: LifeShare Blood Centers, Shreveport, LA, USA. jmmoulds@lifeshare.org Prof ML Olsson: Blood Centre, University Hospital, Lund, Sweden. Martin_l.Olsson@med.lu.se Dr MAM Overbeeke: Sanquin Blood Supply, Diagnostic Services, Amsterdam, the Netherlands. m.overbeeke@sanquin.nl Ms J Poole: IBGRL, NHS Blood and Transplant, Filton, Bristol, UK. joyce.poole@nbs.nhs.uk Dr ME Reid: New York Blood Center, New York, NY, USA. mreid@nybloodcentre.org Prof Ph Rouger: Centre national de Référence pour les Groupes sanguines, Paris, France. tcb_ints@ints.fr Prof CE van der Schoot: Sanquin Research at CLB, Amsterdam, the Netherlands. e.vanderschoot@sanquin.nl Prof M Scott: Bristol Institute for Transfusion Sciences, NHS Blood and Tranplant, Filton, Bristol, UK. marion.scott@nbs.nhs.uk Dr P Sistonen: Finnish Red Cross Blood Transfusion Service, Helsinki, Finland. pertti.sistonen@bts.redcross.fi Mrs E Smart: Durban, South Africa. eapsmart@svnet.co.za Dr JR Storry: Blood Centre, University Hospital, Lund, Sweden. jill.storry@med.lu.se Dr Y Tani: Osaka Red Cross Blood Center, Osaka, Japan. taniy@sannet.ne.jp Dr LC Yu: Mackay Memorial Hospital and National Taiwan University, Taipei, Taiwan. yulc@ntu.edu.tw Dr S Wendel: Blood Bank, Hospital Sirio-Libanes, São Paulo, Brazil. snwendel@uninet.com.br Dr CM Westhoff: American Red Cross and the University of Pennsylvania, Philadelphia, PA, USA. westhoff@usa.redcross.org Dr V Yahalom: NBGRL Magen David Adom, Ramat Gan, Israel. veredy@mdais.co.il Dr T Zelinski: Rh Laboratory, Winnipeg, Manitoba, Canada. zelinski@ms.umanitoba.ca
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