An alloantibody to a highprevalence MNS antigen in a person with a GP.JL/Mk phenotype

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Immunohematology

American National Red Cross

Subject: Medical Laboratory Technology

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ISSN: 0894-203X
eISSN: 1930-3955

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VOLUME 23 , ISSUE 4 (December 2007) > List of articles

An alloantibody to a highprevalence MNS antigen in a person with a GP.JL/Mk phenotype

John Ratliff / Susan Veneman / Joan Ward / Christine Lomas-Francis / Kim Hue-Roye / Randall W. Velliquette / Laima Sausais / Twilla Maldonado / Janet Miyamoto / Yolanda Martin / David Slater / Marion E. Reid

Keywords : MNS blood group system, glycophorin, blood groups, alloantibody, high-prevalence antigen

Citation Information : Immunohematology. Volume 23, Issue 4, Pages 146-149, DOI: https://doi.org/10.21307/immunohematology-2019-332

License : (Transfer of Copyright)

Published Online: 01-April-2020

ARTICLE

ABSTRACT

The low-prevalence MNS blood group antigenTSEN is located at the junction of glycophorinA (GPA) to glycophorin B (GPB) in several hybrid glycophorin molecules. Extremely rare people have RBCs with a double dose of theTSEN antigen and have made an antibody to a high-prevalence MNS antigen. We report the first patient who is heterozygous for GYP.JL and Mk. During prenatal tests,an alloantibody to a high-prevalence antigen was detected in the serum of a 21-year-old Hispanic woman. The antibody detected an antigen resistant to treatment by papain, trypsin,α-chymotrypsin, or DTT. The antibody was strongly reactive by the IAT with all RBCs tested except those having the MkMk, GP.Hil/GP.Hil, or GP.JL/GP.JL phenotypes. The patient’s RBCs typed M+N–S+/–s–U+, En(a+/–), Hut–, Mi(a–), Mur–, Vw–, Wr(a–b–), and were TSEN+, MINY+. Reactivity with Glycine soja suggested that her RBCs had a decreased level of sialic acid. Immunoblotting showed the presence of monomer and dimer forms of a GP(A-B) hybrid and an absence of GPA and GPB. Sequencing of DNA and PCR-RFLP using the restriction enzyme RsaI confirmed the presence of a hybrid GYP(AB). The patient’s antibody was determined to be anti-EnaFR. She is the first person reported with the GP.JL phenotype associated with a deletion of GYPA and GYPB in trans to GYP.JL.

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