C O N T E N T SSee AlsoDescriptionA class of chemicals, called the Immunoglobulins, made by the cells of the immune system to specifically tag or identify foreign material within the body of the host. Antibodies combine with specific markers Antigens found on viruses, bacteria, or other toxins, and agglutinate them. The immune system is capable of manufacturing millions of different antibodies against a wide variety of potential invaders. Individuals of Type O, Type A, or Type B blood carry Antibodiesto other blood types. Type AB, the universal recipient, manufactures no Antibodies to other types. Discussion
Antibodies to A and BOrdinarily, people possess antibodies directed toward the A or B antigen absent from their own RBCs. This predictable complimentary relationship permits serum grouping in addition to RBC ABO grouping tests . The immunoreactive configurations that confer A and B specificities to molecules of the RBC membrane also exist in other biologic entities, notably bacterial cell walls. Bacteria are widespread in the environment and it appears that their presence in intestinal flora, dust, food and other widely distributed agents ensure a constant exposure of all persons to A-like and B-like antigens. Immunocompetent persons react to the environmental antigens by producing antibodies to those that are absent in their own systems. Thus, anti-A occurs in the sera of group O and group B persons and anti-B occurs in the sera of group O and group A persons. Group AB people, having both antigens, make neither antibody. Time of AppearanceAnti-A and anti-B production generally begins after the first few months of life. Occasionally infants can be found that are already producing these antibodies at the time of birth. Antibody production remains fairly constant until late in adult life. In elderly people, anti-A and anti-B levels may be lower than those seen in young adults. Since antibody production normally begins after birth, results that are obtained with the sera of newborns or infants to about 4-6 months cannot be considered valid because the antibodies may have been acquired through the placental transfer of maternal IgG anti-A and anti-B.
Reactivity of Anti-A and Anti-BAnti-A produced by group B persons and anti-B produced by A people are composed predominantly of IgM molecules. Small quantifies of IgG molecules are also present in the sera of these two groups. IgG is the dominant form of anti-A and anti-B of group O serum. The IgG forms readily cross the placenta and can cause ABO hemolytic disease of the newborn (HDN). Because of the predominance of IgM antibodies in the sera of group A or B persons, ABO hemolytic disease is rarely seen in ABO-incompatible infants born of group A or B mothers. The distinguishing features of IgM and IgG anti-A and anti-B are given in Table 10-3. Both immunoglobulin types preferentially agglutinate red cells at room temperature (20-25 C) or below. Both are efficient activators of complement at 37 C. The complement-mediated lytic capabilities of these antibodies are most apparent when an incubation phase at 37 C is added to serum grouping tests. Occasionally, patients or donors can be found whose sera cause the hemolysis of ABO-incompatible red cells at temperatures below 37 C. Hemolysis by ABO antibodies in serum grouping tests should be suspected when a pink to red discoloration appears in the supernates or when the buttons of reagent ABO grouping RBCs are reduced in size or are missing. Hemolysis must be interpreted as a positive result. Hemolysis of RBCs will not occur if reagent RBCs are suspended in solutions that contain EDTA or other anticoagulants that prohibit complement activation. Agglutinin development and cause“It is difficult to understand how agglutinins are produced in individuals who do not have the respective antigenic substances in their red blood cells. However, small amounts of group A and B antigens are believed to enter the body in the food, in bacteria, or by other means, and these substances presumably initiate the development of anti-A or anti-B agglutinins.” -Guyton, Textbook of Medical Physiology Anti-A,B (Group O Serum)Serum from group O persons contains an antibody designated as anti-A,B. It reacts with A and B RBCs and activities for both RBC groups cannot be separated by differential adsorption. Eluates prepared from group A RBCs that have been used to adsorb group O serum contain anti-A and an antibody that reacts with both A and B RBCs. Similar findings are obtained when B RBCs are used for adsorption. Saliva from A or B secretors inhibits the activity of this antibody with either A or B RBCs. Anti-A1The anti-A of group B serum appears, from simple studies, to contain separable anti-A and anti-A1. In direct tests, group B serum agglutinates A1 and A2 RBCs, yet following adsorption with A2 RBCs, group B serum reacts only with A1 RBCs. If further tests are performed, the differences between A antigen expression on A1 and A2 RBCs appears to be quantitative rather than qualitative. Further adsorption of group B serum with A2 RBCs will remove all serum activity for A1 RBCs. The apparent anti-A1 made by adsorption of group B serum can be thought of as a weakened form of anti-A. It reacts with A1 RBCs because they have more A antigen than do A2 RBCs. The sera of persons of certain weak subgroups of A may contain anti-A1 that is serologically similar to the anti-A1 of group B adsorbed serum. Adsorbed group B serum can be used at the practical level to differentiate the two common A subgroups. More frequently, however, anti-A, reagents are employed that are manufactured from the lectin of Dolichos biflorus. The lectin will react with A, and A2RBCs unless it has been diluted appropriately. Reagent anti-A, lectins have been diluted by the manufacturer to react with & but not A2, RBCs. IgA, IgG and IgM anti-blood group A antibodies induced by pneumococcal vaccineKoskela P, Nurmi T, Haiva VM Vaccine 1988 Jun;6(3):221-222 National Public Health Institute, Kuopio, Finland.
Characteristics of anti-A and anti-B in black ZimbabweansVox Sang 1994;67(3):307-309 Adewuyi JO, Gwanzura C, Mvere D Department of Haematology, University of Zimbabwe, Harare.
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