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Alloagglutinins of M and N specificites with unique characteristics found in normal sera are described. Specific M or N agglutination by these sera occurred only when erythrocytes had been exposed to glucose-containing solutions. Conversion to the form of MN recognized by these sera required incubation of the cells in 1 to 2% glucose buffered to physiological or alkaline pH and was dependent on time and temperature of exposure, occurring in hours at 37 C and in days at 4 C. The sera appeared to be detecting an antigenic structure in which interaction between glucose and the amino group of the N-terminal amino acid of the MN receptor has produced a new specificity, analogous to the action of formaldehyde on N receptors and the resulting N-like structure detected by sera from hemodialysis patients.

A third Finnish En(a-) individual (ERP) with alloanti-Ena has been identified. Subsequent family studies revealed that ERP is distantly related to the 2 previous Finnish En(a-) propositi. Serologically, ERP's erythrocytes were found to be M-N-'N'+S-s+U+En(a-)Wr(a-b-) and were sialic acid deficient. SDS-PAGE studies confirmed that the red cell membranes lacked the MN-sialoglycoprotein, glycophorin-A. ERP's serum contained an IgG antibody which demonstrated two separable specificities, a ficin-sensitive specificity (anti-EnFS) and a ficin-resistant specificity (anti-EnFR), which reacted by the indirect antiglobulin technique. The antibodies were probably pregnancy induced, as ERP had never been transfused. A 51Cr-labelled red cell survival study showed that the antibodies were capable of causing significant destruction of incompatible red cells.

This report presents the first prospectively followed case of hemolytic disease of the newborn due to anti-Jk3 alone. A Samoan woman with known anti-Jk3 was closely monitored during her third pregnancy. Because of elevated delta OD values in the amniotic fluid and rising titer of serum antibody, labor was induced at 36 weeks gestation. The cord red blood cells were coated with IgG, and anti-Jk3 was eluted from the cord cells and the placenta. A family study was done quantitating the expression of Kidd antigens by titrations and scores. Although titrations and scores have been reported to identify cells carrying the silent allele Jk in the heterozygous state, in this family, dosage differences were noted with only 1 of 2 Jk-heterozygous daughters.

This extraordinary case showcases the identification of a rare anti-En a specificity that was assisted by DNA-based red blood cell antigen typing and collaboration between the hospital blood bank in the United States, the home blood center in Qatar, the blood center Immunohematology Reference Laboratory, as well as the American Rare Donor Program (ARDP) and the International Society for Blood Transfusion (ISBT) International Rare Donor Panel. En a is a high-prevalence antigen, and blood samples from over 200 individuals of the extended family in Qatar were crossmatched against the patient's plasma with one compatible En(a-) individual identified. The ISBT International Rare Donor Panel identified an additional donor in Canada, resulting in a total of two En(a-) individuals available to donate blood for the patient., (© 2024 Stella T. Chou et al., published by Sciendo.)

Abstract: Regular blood transfusion is the cornerstone of care for patients with red blood cell (RBC) disorders such as thalassaemia or sickle‐cell disease. With repeated transfusion, alloimmunisation often occurs due to incompatibility at the level of minor blood group antigens. We use CRISPR‐mediated genome editing of an immortalised human erythroblast cell line (BEL‐A) to generate multiple enucleation competent cell lines deficient in individual blood groups. Edits are combined to generate a single cell line deficient in multiple antigens responsible for the most common transfusion incompatibilities: ABO (Bombay phenotype), Rh (Rhnull), Kell (K0), Duffy (Fynull), GPB (S−s−U−). These cells can be differentiated to generate deformable reticulocytes, illustrating the capacity for coexistence of multiple rare blood group antigen null phenotypes. This study provides the first proof‐of‐principle demonstration of combinatorial CRISPR‐mediated blood group gene editing to generate customisable or multi‐compatible RBCs for diagnostic reagents or recipients with complicated matching requirements. [ABSTRACT FROM AUTHOR]

Background: The Kidd-null phenotype, Jk(a-b-), occurs in individuals who do not express the JK glycoprotein. Jk(a-b-) individuals can make an antibody against the Jk3 antigen, a high-incidence antigen present in more than 99.9% of most populations. This presents many challenges to the blood bank including identification of the antibody, masking of other antibodies, and how to provide transfusion support given the rarity of Jk3-negative blood products. Kidd antibodies may cause acute and delayed hemolytic reactions as well as hemolytic disease of the fetus and newborn (HDFN). In this article, we present a series of four practical cases of pregnant women with the anti-Jk3 alloantibody that demonstrate a range of clinical presentations of Kidd-related HDFN.Study Design and Methods: We retrospectively reviewed the clinical and blood bank records for four patients and their newborns encountered at institutions in Tennessee, Missouri, Hawaii, and Guam with an anti-Jk3 identified during pregnancy.Results: Two cases showed no significant evidence for HDFN, while two cases were of mild-to-moderate severity requiring early delivery due to elevated middle cerebral artery (MCA) flow velocities but requiring only phototherapy for hyperbilirubinemia. No intrauterine or neonatal transfusions were necessary. Anti-Jk3 alloantibody titers ranged from 2 to 128.Conclusion: Clinical manifestations of anti-Jk3 HDFN are generally mild to moderate. Anti-Jk3 titers were not found to correlate directly with HDFN severity. We suggest a titer of 16 to 32 as a cutoff for implementing enhanced monitoring of fetal MCA flow velocities, as such titers may be indicative of elevated HDFN risk. [ABSTRACT FROM AUTHOR]

Background and Objectives Rh blood group system is one of the complex systems of blood groups and composed of nearly 50 antigens. The two gens of Rh D and Rh CE are responsible for coding of Rh system. Rh null genotype does not express any of these antigens. The prevalence of phenotype Rh null is 1 person per every 6×106 individuals and it is rather difficult to find compatible blood for the recipients in need. However, as there are probably members with similar characteristics in a given family, it would be plausible to diagnose the phenotype in family members to prepare compatible blood in time of need. Case In 2014, a 39-year-old negative female patient with hemolytic anemia referred to BoAli Hospital in Qazvin. Her sample, due to incompatibility in cross matching was further tested and her Rh null group was determined. Conclusions This case was identified by antibody screening tests and the subsequent determination of Rh antigen phenotype. After checking other family members, her brother was identified as the second Rh null group case in the country. [ABSTRACT FROM AUTHOR]

Accurate typing of a patient's RBCs in the setting of prior transfusion or a hemolytic transfusion reaction is crucial in the selection of compatible blood but is time consuming, technically difficult, and sometimes impossible. To address this problem, a simple, rapid, and inexpensive quantitative PCR method was developed to identify the single nucleotide polymorphism (SNP) of the Kidd blood group. We applied this method in a clinical investigation of 54 multiple-transfusion patients. Patients were eligible if they had received at least one RBC transfusion within 30 days and had a sample referred to our regional reference lab for assistance with compatibility testing requiring reticulocyte separation, hypotonic saline treatment, or chemical modification to remove IgG. We compared serologic result to the normalized quantitative PCR. For discrepants, or where no serologic type could be assigned, DNA sequencing characterized the patient's Kidd SNP. Of the 54 patients, the reference lab could assign a serologic Kidd type for 33. Quantitative PCR assigned a Kidd type for 53 of the 54. In three cases, where serology and PCR were discrepant, and for all cases where serology could not assign a Kidd type, DNA sequencing verified the Kidd typing assigned by PCR. A simple, rapid, and accurate technique has been developed. The assay performs well in the clinical setting. With further study, and inclusion of other blood group systems, this may become an important supplemental technique for selected patients in the immunohematology reference laboratory. [ABSTRACT FROM AUTHOR]

The Mep/Amt proteins constitute a new family of transport proteins that are ubiquitous in nature. Members from bacteria, yeast and plants have been identified experimentally as high-affinity ammonium transporters. We have determined the topology of AmtB, a Mep/Amt protein from Escherichia coli , as a representative protein for the complete family. This was established using a minimal set of AmtB–PhoA fusion proteins with a complementary set of AmtB–LacZ fusions. These data, accompanied by an in silico analysis, indicate that the majority of the Mep/Amt proteins contain 11 membrane-spanning helices, with the N-terminus on the exterior face of the membrane and the C-terminus on the interior. A small subset, including E. coli AmtB, probably have an additional twelfth membrane-spanning region at the N-terminus. Addition of PhoA or LacZ α-peptide to the C-terminus of E. coli AmtB resulted in complete loss of transport activity, as judged by measurements of [14 C]-methylammonium uptake. This C-terminal region, along with four membrane-spanning helices, contains multiple residues that are conserved within the Mep/Amt protein family. Structural modelling of the E. coli AmtB protein suggests a number of secondary structural features that might contribute to function, including a putative ammonium binding site on the periplasmic face of the membrane at residue Asp-182. The implications of these results are discussed in relation to the structure and function of the related human Rhesus proteins. [ABSTRACT FROM AUTHOR]

We report a case with hydrops fetalis resulting from homozygous α-thalassemia and alloimmune hemolytic anemia due to anti-JK3. This is one of the few cases with immune- and nonimmune-induced hydrops fetalis Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The article presents a case study of a 39-year-old G3P2 Burmese woman with anti-JK3 antibody during pregnancy. Topics mentioned include the indirect antiglobulin test (IAT) used to detect the antibody, the DNA analysis, and the importance of serologic testing. Also mentioned are the peripheral white blood cells analysis and the hemolytic disease of the fetus and newborn (HDFN) associated with JK3 antibody.