Many components of human plasma can be antigenic when whole blood or plasma is transfused. Problems associated with such antibodies represent one of the less well-investigated areas in blood transfusion. Urticarial reactions following the transfusion of blood or plasma components are not infrequent, although the culprit proteins are only rarely disclosed and are most likely to be ingested haptens present in donor plasma (e.g. chocolate, drugs). Quite often the antibodies causing the reactions are IgE. Antibodies to factor VIII are not known to cause transfusion reactions, although they will cause inhibition of the activity of transfused factor VIII. Antibodies to IgA can lead to serious anaphylactic reactions. Antibodies to IgG determinants may cause problems in blood grouping, but their role in transfusion reactions is debatable.
Gm antigens are polymorphic antigens on the heavy chains of IgG (y-chains), present mainly on the Fc fragment, although a few are on the Fd fragment. There are many different Gm antigens and they are inherited in haplotypes. IgG myeloma proteins have shown that different Gm antigens are associated with different IgG subclasses (e.g. IgG1 can carry four different Gm determinants, whereas IgG3 can carry 13 and IgG4 none).
Typing for Gm antigens is carried out with test serum to inhibit the agglutination of red cells coated with selected IgG Rh antibodies, of known Gm status, by Gm-specific antibodies.
Gm antibodies are found in: (i) the sera of patients with rheumatoid arthritis; (ii) the sera of women who have been pregnant; (iii) children between the age of 6 months and 5 years who are Gm incompatible with their mothers' IgG; and (iv) some normal adults. Gm antibodies are of no significance in transfusion medicine.
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