Marion E. Reid

TSEN: A Novel MNS-Related Blood Group Antigen

We report an antibody (anti‐TSEN) that recognizes an antigen (TSEN) at the unique amino acid sequence that results from the junction of GPA58 to GPB27 if the GPB carries the S antigen. Red cells from several unrelated donors that possess this specific GP(A‐B) hybrid molecule were agglutinated by anti‐TSEN. Since a synthetic peptide with the amino acid sequence at this junction (Pro‐Glu‐Glu‐Glu‐Thr‐Gly‐Glu‐Met‐Gly‐Gln‐Leu‐Val‐His‐Arg) specifically inhibited anti‐TSEN, it must detect an antigen within this novel amino acid sequence. The TSEN antigen has been provisionally assigned the MNS blood group system number 002.033 on behalf of the ISBT Working Party on Terminology for Red Cell Surface Antigens.

Does Anti‐Jra Cause Hemolytic Disease of the Newborn?

Abstract. A Jr(a‐) Japanese female developed anti‐Jra during her first pregnancy. Both father and infant red cells were Jr(a+), and anti‐Jra was eluted from the infants red cells. The antibody was determined to be IgGl. Hemolysis could not be definitively established from the clinical data. The pitfall of using the presence of jaundice as the sole evidence for hemolysis is emphasized. We conclude that the present case, and other previously reported cases, do not unequivocally establish that anti‐Jra causes significant hemolytic diesease of the newborn (HDN). Amniocentesis probably should not be performed during the pregnancy of mothers sensitized to Jra antigen. Jra HDN is probably a mild disease, like ABO HDN.

RHCE*ceMO is frequently in cis to RHD*DAU0 and encodes a hr(S) -, hr(B) -, RH:-61 phenotype in black persons: clinical significance.

RHCE*ceMO has nucleotide changes 48G>C and 667G>T, which encode, respectively, 16Cys and 223Phe associated with altered expression of e antigen. RHD*DAU0 has Nucleotide 1136C>T, which encodes 379Met associated with normal levels of D. We compiled serologic and DNA testing data on samples with RHCE*ceMO to determine the red blood cell (RBC) antigen expression, antibody specificity, RHD association, and the prevalence in African‐American persons.

Autoantibodies Mimicking Anti‐Jkbplus Anti‐Jk3 Associated with Autoimmune Hemolytic Anemia in a Primipara Who Delivered an Unaffected Infant

Abstract. A serum sample from a nontransfused 2 5‐year‐old Caucasian primipara contained weak anti‐Jkbplus anti‐Jk3. The direct antiglobulin test on the patients red cells was strongly positive. Anti‐Jkbwas recovered in a heat eluate. An ether eluate contained anti‐Jk3. Her red cells typed as Jk(a‐b+)Jk:3. The anti‐Jkband anti‐Jk3 reactivity was completely absorbed both by red cell samples lacking and red cells possessing the corresponding antigens, indicating these antibody specificities to be of the mimicking variety. At 41 weeks gestation she delivered a normal, healthy infant with no detectable serum or cell bound antibody.

Characteristics of an antibody causing agglutination of M-positive non-enzymatically glycosylated human red cells.

An alloagglutinin was identified in the serum of an M‐negative diabetic patient. The agglutinin reacted with all commercial M‐positive red cell samples. Routine cross‐matches showed no incompatibility. This anti‐M would only agglutinate M‐positive red cell samples that had been incubated in 2% glucose for a minimum of 2 h at 37°C, 2 days at 22°C, or 1 week at 4°C. Reactive red cell samples, when washed and incubated in saline, gradually became non‐reactive. This antibody reacted optimally in low ionic strength solution at 16°C for 20 min where MM red cells were agglutinated to a titer of 256, score 85; and MN red cells were agglutinated to a titer of 128, score 66. The antibody was denatured by 2‐mercaptoethanol and was inhibited by a crude M tryptic isolate and by 2 % glucose, but not by other sugars prepared at a 2% concentration.

Auto-anti-A1: another cause of ABO discrepancy.

Anti‐A1 was found in the serum of a patient of blood group A1 who had never received a blood transfusion. The patients serum caused agglutination of his own red blood cells. The anti‐A1 could be totally absorbed by red blood cells from the patient and from other A1 individuals. The anti‐A1 was inhibitable by soluble group A‐specific substance and was denatured by 2‐mercaptoethanol. The A and H serum transferases were normal. The presence of auto‐anti‐A1 in the serum of an A1 individual is yet another cause of ABO discrepancy.

A Private Red Cell Antigen, Jones, Causing Haemolytic Disease of the Newborn

Abstract. Two previously unpublished low‐incidence antigens, Jones and Hol., are identical. The antigen is a dominant, autosomally inherited character that segregates independently from the loci for the ABO, MNS, Duffy and Yt blood group systems and is different from previously published infrequent antigens. The antigen is apparently unaffected by enzyme treatment and is well developed on red cells of neonates. The antibody reacts best by indirect antiglobulin testing, is IgG and has caused haemolytic disease of the newborn. This private blood group antigen, named Jones, has been assigned the ISBT number 700047.