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Biomedical subjects

A Lubenko

Publications and source records attributed to A Lubenko.

18 recordsLinked to original sources
PubMed1992

Molecular biology for platelet alloantigen typing.

Hitherto, full investigation of patients with alloimmunization to platelet-specific antigens has been difficult due to the limited availability of both typing reagents and panels of typed platelets. Following recent advances in the understanding of the molecular and genetic basis of platelet alloantigens, it is now possible to genotype individuals for the alleles coding for the epitopes of four platelet antigen systems (HPA-1-4). This is based on the finding that the two alleles differ by only a single base pair substitution, resulting in one amino acid difference in the relevant platelet glycoprotein. The technique involves amplification of the relevant segments of genomic DNA from any nucleated cell by the polymerase chain reaction, followed by restriction fragment length polymorphism analysis. The technique allows investigation of thrombocytopenic individuals and fetuses/neonates, and can be readily applied to large-scale typing of platelet donors.

Alleles↗
PubMed1992

Haemolytic disease of the newborn probably due to anti-ELO, an antibody to a low frequency red cell antigen.

Investigation of mild bilirubinaemia and a positive direct antiglobulin test in a 2 day old baby revealed that the mother's serum contained an antibody against the low frequency antigen ELO, which was present on the father's red cells. Family studies showed that the ELO antigen segregates from Rh, Gc, ADA and PGM1. The ELO antigen is enzyme resistant and therefore not likely to be part of the MNS or Duffy systems. No abnormalities were detected in immunoblotting studies. Although insufficient samples were available to attempt elution of the antibody from the cord cells, it is probable that this case represents the first reported haemolytic disease of the newborn due to anti-ELO.

Adult↗
PubMed1992

Severe haemolytic disease in an infant born to an Rh(null) proposita.

A 35-year-old Brazilian woman (gravida 4, para 2) was delivered of a severely anaemic child whose cord red blood cells had a strongly positive direct antiglobulin test and who required two exchange transfusions within 24 h of birth. Because of the emergency of the situation and the lack of a local immunohaematology reference laboratory, the phenotype of the mother and the specificity of the relevant antibody could not be determined. Hence, compatible blood was not immediately available and the infant had to be given repeated exchange transfusions with incompatible group 0 Rh-negative blood. The infant is now healthy and thriving. The mother's red cells were subsequently found to lack all the antigens of the Rh system, and her serum reacted with all red cell samples except those of two unrelated Rh(null) individuals. Her serum gave high titres (i.e. 1,024-4,096) by the indirect antiglobulin test against red cells of normal Rh phenotype, as well as against cells with partially deleted Rh phenotypes (titres = 128-512 with -D-/-D- and .D./.D. samples, respectively), and was extremely active in antibody-dependent cell-mediated cytotoxicity and monocyte monolayer assays against red cells of normal Rh phenotypes.

Adult↗
PubMed1992

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.

Adult↗
PubMed1992

Western blotting is a sensitive technique for the detection of anti-PlA1.

Western (immuno-) blotting was evaluated as a technique for anti-PlA1 detection, using untreated and chloroquine or low pH-treated platelets. Chloroquine-treated platelet membranes generated the cleanest blots, giving end-point titres of 4000-16,000 for three different anti-PlA1 sera. These titres were between three and eight doubling dilutions higher than those obtained in solid phase, ELISA or indirect immunofluorescence tests. Nitrocellulose strips used for blotting could be stored for at least six months at room temperature without significant loss of PlA1 activity. However, immunoblotting still failed to detect anti-PlA1 in the sera of four of fivePl (A1-) women whose infants were born with neonatal thrombocytopenia of probable alloimmune origin.

Antibodies↗
PubMed1991

A new qualitative variant of the RhE antigen revealed by heterogeneity among anti-E sera.

We have recently detected a new qualitative variant of the RhE antigen characterised by negative reactions with a minority of anti-E sera, and an inability of the relevant cells to completely absorb most, if not all, anti-E samples that we tested. In tube tests, using a two-stage enzyme technique, cells from the proposita (V.R.) were completely agglutinated by 8 out of 12 undiluted polyclonal sera, weakly agglutinated (2+ and 3+ reactions) by 2 sera, but not agglutinated by the 2 remaining sera. Cross-absorption tests using 1 non-reacting, 1 weakly reacting and 4 strongly reacting polyclonal anti-E sera showed that V.R.'s cells only slightly reduced their anti-E titres versus r"r cells, whilst completely removing their reactivity against her own cells. Absorptions with R2R2 cells abolished activity against both cell types. The cells of V.R. failed to absorb or elute anti-Ew, and had normal expression of c. Three monoclonal human anti-E reagents were tested by fluorescence flow cytometry; one reagent failed to react with the cells of V.R., a second bound as strongly with V.R.'s cells as with R1R2 controls while the third bound much more weakly with V.R. than with any other E+ sample. The variant of RhE in the V.R. family is therefore distinct from Ew, and lacks an epitope recognised by a major constituent of most anti-E sera. This epitope is unlikely to be ET, since all of 91 samples from E-positive Australian aborigines (many of which are expected to lack ET) were agglutinated by a serum that failed to react with V.R.'s cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Agglutination Tests↗
PubMed1989

Should anti-Rh immunoglobulin be given D variant women?

D variant women occasionally form anti-D during or following pregnancy with a D-positive fetus. It is not known whether Rh immunization could be suppressed by using anti-Rh immunoglobulin (Rh Ig), or whether the injected antibodies would be absorbed by the woman's D variant cells. In order to predict the likely outcome, three anti-Rh Ig preparations were absorbed independently with five examples of D variant red cells: R1VIr (n = 3), R1Br (n = 2), and with cells of common Rh-positive and Rh-negative phenotypes: R0, r'r, r"r or rr cells (n = 1 each). The titres of the Ig preparations against all these cells were compared after three, six, nine and 12 absorptions. The titres of the unabsorbed anti-Rh Igs against R0 cells ranged from 2(15) to 2(18). Anti-D activities were hardly affected by absorption with r'r, r"r or rr cells, but were completely exhausted after three to six absorptions with R0 cells. Most of the D variant cells were as ineffective as rr cells in reducing anti-D activity against R0 cells, but one R1VIr variant produced a fall in titre against R0 cells, equivalent to four or five doubling dilutions after three to six absorptions, which could not be reduced further by subsequent absorptions. Therefore, a substantial proportion of the anti-D in the immunoglobulin preparation does not bind to D variant red cells. The component of the anti-D that does not bind to D variant cells would be expected to be present in the circulation of D variant individuals injected with anti-Rh immunoglobulin, and should be effective in suppressing Rh immunization. An increased dose of the anti-Rh Ig might have to be administered in order to allow for the fraction that can bind to D variant red cells and which would not be available for immunosuppression.

Absorption↗
PubMed1989

Analysis of the heterogeneity of the binding site specificities of hyperimmune human anti-A and -A, B sera: the application of competition assays using murine monoclonal antibodies.

Monoclonal antibodies PL41 and AL62 have previously been shown to recognize two distinct blood group A epitopes on the red cell surface. Competitive inhibition of the binding of 125I-PL41 and 125I-AL62 to group A1 red cells, by hyperimmune polyclonal human antibodies, has been employed to investigate the binding site specificities of 15 anti-A and 8 anti-A,B sera. Differences in the degree of inhibition of the binding of the two MABs by individual anti-A or -A,B samples indicate that polyclonal reagents are composed of varying proportions of up to 3 (or more) different antibody specificities, each recognizing a distinct epitope: PL41-like, AL62-like and a third (as yet undefined) category of antibody. In general, those anti-A sera with PL41-like specificities are superior agglutinators of A2B cells with weakly expressed A antigens; similarly, the specificity of potent anti-A,B, sera capable of strongly agglutinating Ax cells was likewise directed towards PL41-binding blood group A trisaccharide haptens.

ABO Blood-Group System↗
PubMed1989

Kg, a new low-frequency red cell antigen responsible for hemolytic disease of the newborn.

Hemolytic disease of the newborn in a Japanese infant led to studies which indicate that an antibody detected in the maternal serum is recognizing a hitherto unknown red cell antigen. The antigen, which we have named Kg, was found in two generations of the family and it is inherited as a Mendelian dominant character. The maternal serum failed to react with the red cells of more than 600 random Japanese blood donors, 64 red cell samples known to possess low-frequency antigens and all but one of 75 red cell samples known to lack high-frequency antigens without recognized low-frequency antigens. The father's red cells were tested extensively for established low-frequency antigens; only Dia was demonstrated and the maternal antibody was shown not to contain anti-Dia.

ABO Blood-Group System↗
PubMed1986

Epitope specificity of blood-group-A-reactive murine monoclonal antibodies.

Monoclonal antibodies (MABs) towards blood groups A manifested three broad patterns of binding distinguished on the basis of affinities for A1 or A2B phenotype red blood cells and blood group substances. Competitive inhibition of binding of radiolabelled MABs by other unlabelled antibodies and absorption studies with synthetic haptens suggested that GpA specificity was expressed as two topographically related structures, one being the terminal GpA trisaccharide and the second probably involving part of the oligosaccharide backbone. The enhancement of binding of an extremely low-affinity antibody by higher affinity antibodies recognising either epitope indicated a topographic, possibly conformational relationship between these epitopes. It is suggested that only those antibodies that recognise terminal GpA trisaccharides can agglutinate weak A2B cells.

ABO Blood-Group System↗
PubMed1979

The incidence of antibodies to low frequency antigens (LFA) in plasmapheresis donors with hyperimmune Rh antisera.

Over 50% of plasmas from plasmapheresis donors hyperimmunized for Rh antibodies were found to contain antibodies to low frequency red cell antigens (LFA). The majority of these plasmas contained antibodies to more than one LFA. On the other hand, the incidence of these antibodies in immune plasma from control plasmapheresis donors was markedly lower. The significance of the high incidence of these antibodies in grouping reagents is discussed.

Antibodies↗
PubMed1978

Further data on the Pta antigen.

The second Pt(a+) family is described. Pta is shown to segregate independently from several genetic markers.

ABO Blood-Group System↗
PubMedDate not supplied

A serologic relationship among the NFLD, BOW, and Wu red cell antigens.

A survey of sera containing antibodies to multiple low-incidence antigens revealed a variety of patterns of reactions with NFLD+, BOW+, and Wu+ red cell samples. Although NFLD, BOW, and Wu are distinct antigenic determinants (International Society of Blood Transfusion numbers 700.37, 700.46, and 700.13, respectively), their ability to absorb and elute "crossreactive" antibodies indicates a serologic and possibly a genetic relationship among the three.

Blood Group Antigens↗