BACKGROUND: KELnull (K0) persons can produce clinically significant anti-KEL5 antibody after transfusion and/or pregnancy, requiring K0 blood transfusion when indicated. 37 K0 alleles have been reported in studies over different populations, but none in Amerindian-Caucasian descendants from South America. The aim of this study was to identify the molecular basis of K0 phenotype in Brazilians. METHODS: We investigated three K0 samples from different Brazilian blood banks (Recife, Manaus, and Vila Velha) in women with anti-KEL5. KEL antigen typing was performed by serologic techniques, and the K0 status was confirmed by flow cytometry. PCR-RFLP and DNA sequencing of the KEL coding and exon-intron regions were also performed. RESULTS: RBCs of the 3 patients were phenotyped as KEL:-1,-2,-3,-4,-7. The 3 patients had the same KEL*02/02 genotype and were negative for KEL*02.03 and KEL*02.06 alleles. The Recife K0 patient was homozygous for IVS16 + 1g>a mutation (KEL*02N.31 allele). The flow cytometry with anti-KEL1, anti-KEL2, anti-KEL3, anti-KEL4, and anti-CD238 confirmed the K0 phenotype. In addition, we found the c.10423C>T mutation (KEL*02N.04 allele) in both the Manaus K0 and the Vila Velha K0 patients. CONCLUSION: This report represents the first study of K0 molecular basis performed in Amerindian-Caucasian descendants from South America.
BACKGROUND: KELnull (K0) persons can produce clinically significant anti-KEL5 antibody after transfusion and/or pregnancy, requiring K0 blood transfusion when indicated. 37 K0 alleles have been reported in studies over different populations, but none in Amerindian-Caucasian descendants from South America. The aim of this study was to identify the molecular basis of K0 phenotype in Brazilians. METHODS: We investigated three K0 samples from different Brazilian blood banks (Recife, Manaus, and Vila Velha) in women with anti-KEL5. KEL antigen typing was performed by serologic techniques, and the K0 status was confirmed by flow cytometry. PCR-RFLP and DNA sequencing of the KEL coding and exon-intron regions were also performed. RESULTS: RBCs of the 3 patients were phenotyped as KEL:-1,-2,-3,-4,-7. The 3 patients had the same KEL*02/02 genotype and were negative for KEL*02.03 and KEL*02.06 alleles. The Recife K0 patient was homozygous for IVS16 + 1g>a mutation (KEL*02N.31 allele). The flow cytometry with anti-KEL1, anti-KEL2, anti-KEL3, anti-KEL4, and anti-CD238 confirmed the K0 phenotype. In addition, we found the c.10423C>T mutation (KEL*02N.04 allele) in both the Manaus K0 and the Vila Velha K0 patients. CONCLUSION: This report represents the first study of K0 molecular basis performed in Amerindian-Caucasian descendants from South America.
Entities:
Keywords:
KELnull alleles; KELnull phenotype; Kell blood group system
Authors: S Lee; D C Russo; A P Reiner; J H Lee; M Y Sy; M J Telen; W J Judd; P Simon; M J Rodrigues; T Chabert; J Poole; S Jovanovic-Srzentic; C Levene; V Yahalom; C M Redman Journal: J Biol Chem Date: 2001-05-24 Impact factor: 5.157
Authors: Randall W Velliquette; Kim Hue-Roye; Christine Lomas-Francis; Barbara Gillen; Jennifer Schierts; Kristie Gentzkow; Thierry Peyrard; Inge von Zabern; Willy A Flegel; Karen Rodberg; Asim K Debnath; Soohee Lee; Marion E Reid Journal: Transfusion Date: 2013-04-08 Impact factor: 3.157
Authors: Christoph Gassner; Frauke Degenhardt; Stefan Meyer; Caren Vollmert; Nadine Trost; Kathrin Neuenschwander; Yvonne Merki; Claudia Portmann; Sonja Sigurdardottir; Antigoni Zorbas; Charlotte Engström; Jochen Gottschalk; Soraya Amar El Dusouqui; Sophie Waldvogel-Abramovski; Emmanuel Rigal; Jean-Daniel Tissot; Caroline Tinguely; Simon M Mauvais; Amira Sarraj; Daniel Bessero; Michele Stalder; Laura Infanti; Andreas Buser; Jörg Sigle; Tina Weingand; Damiano Castelli; Monica C Braisch; Jutta Thierbach; Sonja Heer; Thomas Schulzki; Michael Krawczak; Andre Franke; Beat M Frey Journal: Transfus Med Hemother Date: 2018-07-10 Impact factor: 3.747