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Case report | 27-April-2020

Case report: massive postpartum transfusion of Jr(a+) red cells in the presence of anti-Jra

Jra is a high-prevalence antigen. The rare Jr(a–) individuals can form anti-Jra after exposure to the Jra antigen through transfusion or pregnancy. The clinical significance of anti-Jra is not well established. This study reports a case of a 31-year-old woman with a previously identified anti-Jra who required massive transfusion of RBCs after developing life-threatening postpartum disseminated intravascular coagulopathy. Despite the emergent transfusion of 15 units of Jra untested RBCs

Shan Yuan, Rosalind Armour, Allison Reid, Khaled F. Abdel-Rahman, Michael Phillips, Dawn M. Rumsey, Theresa Nester

Immunohematology, Volume 21 , ISSUE 3, 97–101

Review | 01-December-2019

A review of the JR blood group system

The JR blood group system (ISBT 032) consists of one antigen, Jra, which is of high prevalence in all populations. The rare Jr(a–) phenotype has been found mostly in Japanese and other Asian populations, but also in people of northern European ancestry, in Bedouin Arabs, and in one Mexican. Anti-Jra has caused transfusion reactions and is involved in hemolytic disease of the fetus and newborn. The Jra antigen is located on ABCG2 transporter, a multipass membrane glycoprotein (also known

Lilian Castilho, Marion E. Reid

Immunohematology, Volume 29 , ISSUE 2, 63–68

Article | 15-February-2021

An update on the JR blood group system

Update on the JR System The JR blood group system consists of one antigen, Jra, which is of high prevalence in all populations. Anti-Jra has caused transfusion reactions and been involved in hemolytic disease of the fetus and newborn. The Jra antigen is located on ABCG2 transporter, a multipass membrane glycoprotein, which is encoded by the ABCG2 gene on chromosome 4q22.1. Several null alleles of ABCG2 (nonsense, deletions, and insertions) are responsible for the Jr(a–) phenotype, and the

L. Castilho

Immunohematology, Volume 35 , ISSUE 2, 43–44

Review | 16-October-2019

Clinical significance of antibodies to antigens in the Raph, John Milton Hagen, I, Globoside, Gill, Rh-associated glycoprotein, FORS, JR, LAN, Vel, CD59, and Augustine blood group systems

transfused antigenpositive red blood cells or a transfusion reaction (e.g., anti-P, anti-Jra, and anti-Lan), and/or hemolytic disease of the fetus and newborn (e.g., anti-RHAG4 and anti-Vel)—has been documented. For other antibodies, their prevalence is so rare that information on the clinical significance of their antibodies is not available (e.g., anti-FORS1).

Mostafa Moghaddam, Amir Ali Naghi

Immunohematology, Volume 34 , ISSUE 3, 85–90

Article | 16-November-2020

Effect of pronase on highincidence blood group antigens and the prevalence of antibodies to pronase-treated erythrocytes

Cromer and Lutheran blood group systems and the JMH antigen were sensitive to pronase treatment of RBCs. Antigens in the Dombrock blood group system and Sc1 were either sensitive to or markedly weakened by pronase treatment of RBCs. The following high-incidence antigens were resistant to treatment of RBCs with pronase: AnWj, Ata, Coa, Co3, Dib, EnaFR, Era, Fy3, Jk3, Jra, k, Kpb, Jsb, K14, Lan, Oka, Rh17, U, Vel, and Wrb. Over half of the serum samples from normal blood donors contained antibodies to

Marion E. Reid, Carole A. Green, Jack Hoffer, Ragnhild Øyen

Immunohematology, Volume 12 , ISSUE 4, 139–142

Article | 10-November-2020

Do monocyte ADCC assays accurately predict the severity of hemolytic disease of the newborn caused by antibodies to high-frequency antigens?

;(anti-Hy, -Dib, -Jra, -Sc1, -Inb, -Wrb, and -U [n=2]) had low ADCC activity (< 28%) and did not cause HDN. The IAT titers ranged from 4 to 128. Two antibodies (anti-Ena and anti-Rh29) had high ADCC activity (≥ 72%) and high IAT titers (≥ 1,024), and both caused severe HDN. The remaining four antibodies (anti-Cra, -Inb, and -U [n = 2]) had ADCC activity ≥ 40 percent and titers ≥ 128, but they did not cause HDN. The inability of anti-Cra and anti-Inb to cause HDN is presumed to be

Stephen F. Garner, Alan Devenish

Immunohematology, Volume 12 , ISSUE 1, 20–26

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