BACKGROUND: CD59 is a cell surface glycoprotein of approximately 20 kDa limiting the lytic activity of the terminal complement complex C5b-9. Although CD59 is known as a red blood cell (RBC) antigen defined by monoclonal antibodies, it so far has not been identified as a blood group antigen, since the description of a human alloantibody was missing. In this study we show the presence of an anti-CD59 in a patient affected by a homozygous CD59 deficiency. STUDY DESIGN AND METHODS: RBC CD59 and CD55 were determined by flow cytometry or by the column agglutination technique using monoclonal antisera. Commercially available His-tagged recombinant soluble CD59 protein was used to inhibit anti-CD59. RESULTS: Seven cases of an isolated CD59 deficiency due to three distinct null alleles of the CD59 gene have been published so far. Recently we described the CD59-null allele c.146delA in a young child of heterozygous parents. Her plasma contained an alloantibody directed against the high-prevalence RBC antigen CD59. The antibody specificity was identified using soluble recombinant human CD59 protein, which blocked the reactivity of the patient's antibody and of monoclonal anti-CD59 but not of monoclonal anti-CD55. In addition, RBC alloantibodies such as anti-K, anti-C, anti-c, or anti-Fy(a) remained unaffected. Therefore, inhibition by recombinant CD59 is a useful diagnostic tool to detect alloantibodies in the presence of anti-CD59. CONCLUSION: This is the first demonstration of a human anti-CD59 alloantibody, which defines CD59 as an RBC blood group antigen. CD59 represents a candidate for a new blood group system.
BACKGROUND:CD59 is a cell surface glycoprotein of approximately 20 kDa limiting the lytic activity of the terminal complement complex C5b-9. Although CD59 is known as a red blood cell (RBC) antigen defined by monoclonal antibodies, it so far has not been identified as a blood group antigen, since the description of a human alloantibody was missing. In this study we show the presence of an anti-CD59 in a patient affected by a homozygous CD59 deficiency. STUDY DESIGN AND METHODS: RBC CD59 and CD55 were determined by flow cytometry or by the column agglutination technique using monoclonal antisera. Commercially available His-tagged recombinant soluble CD59 protein was used to inhibit anti-CD59. RESULTS: Seven cases of an isolated CD59 deficiency due to three distinct null alleles of the CD59 gene have been published so far. Recently we described the CD59-null allele c.146delA in a young child of heterozygous parents. Her plasma contained an alloantibody directed against the high-prevalence RBC antigen CD59. The antibody specificity was identified using soluble recombinant humanCD59 protein, which blocked the reactivity of the patient's antibody and of monoclonal anti-CD59 but not of monoclonal anti-CD55. In addition, RBC alloantibodies such as anti-K, anti-C, anti-c, or anti-Fy(a) remained unaffected. Therefore, inhibition by recombinant CD59 is a useful diagnostic tool to detect alloantibodies in the presence of anti-CD59. CONCLUSION: This is the first demonstration of a human anti-CD59 alloantibody, which defines CD59 as an RBC blood group antigen. CD59 represents a candidate for a new blood group system.
Authors: M Yamashina; E Ueda; T Kinoshita; T Takami; A Ojima; H Ono; H Tanaka; N Kondo; T Orii; N Okada Journal: N Engl J Med Date: 1990-10-25 Impact factor: 91.245
Authors: Willy A Flegel; Qing Chen; Lilian Castilho; Margaret A Keller; Ellen B Klapper; William J Lane; France Pirenne; Gary Stack; Maryse St-Louis; Christopher A Tormey; Dan A Waxman; Christof Weinstock; Silvano Wendel; Gregory A Denomme Journal: Blood Transfus Date: 2018-02-14 Impact factor: 3.443
Authors: J R Storry; L Castilho; Q Chen; G Daniels; G Denomme; W A Flegel; C Gassner; M de Haas; C Hyland; M Keller; C Lomas-Francis; J M Moulds; N Nogues; M L Olsson; T Peyrard; C E van der Schoot; Y Tani; N Thornton; F Wagner; S Wendel; C Westhoff; V Yahalom Journal: ISBT Sci Ser Date: 2016-06-27
Authors: William J Lane; Connie M Westhoff; Jon Michael Uy; Maria Aguad; Robin Smeland-Wagman; Richard M Kaufman; Heidi L Rehm; Robert C Green; Leslie E Silberstein Journal: Transfusion Date: 2015-12-03 Impact factor: 3.157