Universal red blood cells—enzymatic conversion of blood group A and B antigens

2004 ◽  
Vol 11 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Martin L Olsson ◽  
Cheryl A Hill ◽  
Humberto de la Vega ◽  
Qiyong P Liu ◽  
Mark R Stroud ◽  
...  
1972 ◽  
Vol 136 (4) ◽  
pp. 799-815 ◽  
Author(s):  
Viktor A. Bokisch ◽  
David Bernstein ◽  
Richard M. Krause

All 110 rabbits immunized with Group A, A-variant, and C streptococcal vaccines produced 19S anti-IgG in addition to antibodies to the streptococcal carbohydrates. 19S anti-IgG was detected by hemagglutination of rabbit red blood cells coated with rabbit anti-blood group F antibody. Antisera of 88 of these animals were also tested for 7S anti-IgG with a coprecipitation assay. This assay is based on the coprecipitation of 7S anti-IgG with complexes of streptococcal carbohydrate and anti-carbohydrate antibody. 50 of the 88 anti-Group C streptococcal antisera contained 7S anti-IgGs. In eight antisera the concentration was greater than 5 mg/ml. The data suggest a genetic influence on the occurrence of 7S anti-IgG. The eight rabbits which produced more than 5 mg/ml of 7S anti-IgG belonged to three related families. Moreover, there were families in which almost every member produced 7S anti-IgG and other families in which only 30% of the members manufactured 7S anti-IgG. The streptococcal vaccine was an especially efficient stimulus for the production of 19S anti-IgG, whereas the pneumococcal vaccine was much less effective in this respect. Furthermore, 7S anti-IgGs were not detected in antipneumococcal antisera, although the concentration of anti-capsular antibodies was similar to that of anti-carbohydrate antibodies in antistreptococcal antisera.


1952 ◽  
Vol 96 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Erwin Neter ◽  
Lee F. Bertram ◽  
Dorothy A. Zak ◽  
Miriam R. Murdock ◽  
Carl E. Arbesman

A study on hemagglutination and hemolysis by Escherichia coli O111 and O55 (rabbit) antisera and on hemagglutination and hemolysis inhibition by E. coli O111 and O55 antigens revealed the following facts. 1. Red blood cells of man, dog, rabbit, guinea pig, sheep, rat, and chicken adsorb E. coli O111 and O55 antigens and thus become specifically agglutinable by the homologous E. coli antisera. 2. The adsorption of these E. coli antigens is a function of the concentration of the antigen, the time (from 5 minutes to 2 hours) of treatment of the red blood cells with the antigen, and the concentration of the red blood cells used. 3. Red blood cells of man and sheep adsorb simultaneously both antigens, as indicated by the fact that both antisera give agglutination of all red blood cells. Complete agglutination does not occur when a mixture of red blood cells treated separately with the two antigens is added to one or the other of the two antisera. 4. Treatment of red blood cells of man with one of the antigens does not block the adsorption of the second antigen. Human cells treated with either or both antigens are still agglutinated by the homologous blood group (A, B, and Rh)-specific antibodies. 5. In the presence of guinea pig complement, E. coli O111 and O55 antisera produce hemolysis of modified human red blood cells in titers of the same order of magnitude as those giving hemagglutination and bacterial agglutination. The same antisera produce hemolysis of sheep cells treated with the identical antigens in titers exceeding by far those giving agglutination of modified human or sheep red blood cells. 6. Both sediment and supernate of a boiled E. coli suspension are capable of modifying red blood cells for E. coli hemagglutination; in contrast, the supernate obtained from an unboiled suspension and then heated does not modify red blood cells for hemagglutination, although it contains the antigen which can specifically adsorb E. coli antibodies, as shown by means of the hemagglutination and hemolysis inhibition tests. 7. Both the unheated and the boiled suspensions of E. coli O111 and O55 inhibit hemagglutination and hemolysis specifically. 8. Rabbit red blood cells modified by either E. coli O111 or 055 antigens, upon intravenous injection into rabbits, engender specific E. coli antibodies. The significance of the results is discussed.


2021 ◽  
Vol 23 (1) ◽  
pp. 17-34
Author(s):  
P. S. Obukhova ◽  
A. V. Kachanov ◽  
N. A. Pozdnyakova ◽  
M. M. Ziganshina

The mother and fetus incompatibility due to Rh-factor, blood group or other blood factors can lead to hemolytic disease of the fetus and newborn (HDN). HDN is a clinical disease condition of the fetus and newborn as a result of hemolysis, when maternal IgG alloantibodies cross the placenta and destroy the red blood cells of the fetus and newborn. The child disease begins in utero and can dramatically increase immediately after birth. As a result, hyperbilirubinemia and anemia develop, that can lead to abortions, serious complications, or death of the neonates in the absence of proper therapy. The range of HDN has changed significantly now compared to previous decades. Half a century ago, HDN was considered an almost complete synonym of RhD-alloimmunization, and this was a frequent problem for newborns. By now due to the high effective of Rh-conflict prevention, immunological AB0-conflicts have become the most common cause of HDN. The review aimes to one of the main causes of jaundice and anemia in neonates at present, i.e. HDN due to immunological AB0-conflict of mother and newborn (AB0-HDN). The main participants of the AВ0- incompatibility mother and child are considered, namely A- and B-glycans, as well as the corresponding anti-glycan alloantibodies. Close attention is paid to the structure features of glycan alloantigens on the red blood cells of the fetus and adult. The possible correlation of the frequency and severity of HDN with the blood group of mother and child, as well as with the titer of maternal alloantibodies, has been considered. The influence of immunoglobulin G subclasses on the AB0-HDN development has been evaluated. In most cases, AB0-HDN appear when the mother has the blood group 0, and the fetus has the group A (subgroup A1) or the group B. Other rare incidences of AB0-incompatibility with severe course are occurred. As a whole the etiology of AB0-HDN is complex and the HDN severity is influenced by many factors. The authors have analyzed statistical data, as well as the prevalence of AB0-incompatibility and AB0-HDN in various regions of the world. Current approaches to the diagnosis of AB0-HDN are discussed in addition. By now the problems of AB0- HDN occurrence and developing of ways to overcome this disease remain relevant.


2000 ◽  
Vol 68 (5) ◽  
pp. 2971-2975 ◽  
Author(s):  
Antonio Barragan ◽  
Peter G. Kremsner ◽  
Mats Wahlgren ◽  
Johan Carlson

ABSTRACT The malaria parasite Plasmodium falciparum utilizes molecules present on the surface of uninfected red blood cells (RBC) for rosette formation, and a dependency on ABO antigens has been previously shown. In this study, the antirosetting effect of immune sera was related to the blood group of the infected human host. Sera from malaria-immune blood group A (or B) individuals were less prone to disrupt rosettes from clinical isolates of blood group A (or B) patients than to disrupt rosettes from isolates of blood group O patients. All fresh clinical isolates and laboratory strains exhibited distinct ABO blood group preferences, indicating that utilization of blood group antigens is a general feature of P. falciparumrosetting. Soluble A antigen strongly inhibited rosette formation when the parasite was cultivated in A RBC, while inhibition by glycosaminoglycans decreased. Furthermore, a soluble A antigen conjugate bound to the cell surface of parasitized RBC. Selective enzymatic digestion of blood group A antigen from the uninfected RBC surfaces totally abolished the preference of the parasite to form rosettes with these RBC, but rosettes could still form. Altogether, present data suggest an important role for A and B antigens as coreceptors in P. falciparum rosetting.


2000 ◽  
Vol 8 (7) ◽  
pp. 3-7
Author(s):  
Stephen W. Carmichael

We are all familiar with the 4 groups of human blood types; 0, A, B, and AB. Each group is characterized by specific molecules on the surface of the red blood cells (RBCs). Recently, Michel Grandbois, Wolfgang Dettmann, Martin Benoit, and Hermann Gaub have modified the atomic force microscope (AFM) to use the different affinities of these molecules to produce an image.A key step was to specifically functionalize the scanning probe tip of the AFM. What this means is to covalently attach an active molecule to the tip. The active molecule they used was a Iectin derived from the snail Helix pomatia (this is the same snail valued by the French as escargot). This Iectin binds specifically to molecules found on the surface of RBCs in blood group A (N-acetylgalactosamine-terminated glycolipids), but these molecules are not found in blood group O. But if the Iectin was bound directly to the AFM tip, nonspecific adsorption to the specimens would occur.


Blood ◽  
1960 ◽  
Vol 16 (2) ◽  
pp. 1163-1172 ◽  
Author(s):  
JØRGEN ANDERSEN

Abstract In a previous paper the author reported investigations of a blood sample (Co) whose blood cells contained, in addition to a normal A antigen, a weak, atypical B-like antigen. The present paper deals with two blood samples, El and Do, which probably possessed the same weak, atypical B-like character. A study of El’s family showed that this blood group character, provisionally designated as Ab, may be inheritable, as it was found in two children and one grandchild of El’s. The serologic studies of the 5 Ab samples are reported, and on the basis of the family material the possible origin of the Ab character is discussed.


2016 ◽  
Vol 14 (3) ◽  
pp. 411-417
Author(s):  
Nguyễn Thị Trung ◽  
Nguyễn Thị Hằng ◽  
Vũ Thị Thu Hằng ◽  
Lê Văn Phan ◽  
Trương Nam Hải

The determination of ABO blood group is obliged in many cases especially before blood transfusion, that is indicated at Point a, Clause 4, Article 14 Circular 26/2013/TT-BYT - Vietnam, date 09.16.2013. For this purpose, both standard sera (monoclonal antibodies) and standard red blood cells are common used but monoclonal antibodies are prefered. In Vietnam, monoclonal antibodies against ABO blood group are not available in domestic production. In this study, we succeeded in the generation of hybidoma cells secreting anti-A monoclonal antibody. Firstly, Balb/c mice were injected with Vietnamese human group A red blood cells to evoke B lymphocyte cells against A antigen present on the surface of the red blood cells. Afterward the lymphocytes were fused with sp2/0 myeloma cells in the presence of polyethylene glycol (PEG) to gain hybrid cells that were identified through ability to expand cells in a selective medium (hypoxanthine aminopterine thymine - HAT) at 37°C and 5% CO2. During screening and isolation process, the positive clones were identified by agglutination test with standard group A red blood cells. Of the 1440 wells, 12 monoclonal hybrid clones were selected. The hybrid cell line (designated A6G11C9) was the best one secreting the highest anti-A monoclonal antibody into culture with the antibody titer of 512. The antibody showed good intensity (+++), and the agglutination was visible by 10 seconds. This antibody is the promising for ABO-grouping kit development.


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