The specificity anti-Gd of human cold autoagglutinins is characterized using
untreated and enzyme-treated human red blood cells. Gd determinants of human RBC are
resistant to proteases, but are inactivated by neuraminidase (RDE). In contrast, I/i determinants
are not inactivated by proteases or RDE, while Pr(1-3) determinants are inactivated by proteases
and RDE, and Pr(a) determinants are resistant to RDE, but are inactivated by proteases.
A monoclonal IgM (y) anti-Pr cold agglutinin occurring after a
rubella infection is shown to have the ‘new’ anti-Pr subspecificity anti-Pr3. Pr3
determinants are found on cat and sheep erythrocytes which lack Prt and Pr2
determinants. By carbodiimide treatment of human erythrocyte glycoproteins,
which causes intramolecular coupling of IV-acetylneuraminic acid carboxyl groups
and nucleophilic centers of the glycoprotein backbone, Pr3 antigen activity is
strongly increased, while Pr, and Pr2 determinants are inactivated.
Coldagglutinins (CA) are autoantibodies against the erythrocyte antigens HI / _ 3 , Pr a and Gd. Anti-l-CA were observed after infection with mycoplasma pneumoniae and cytomegafic virus. The specificity anti-i occurs after infection with Epstein-Barr-Virus. The rare CA followed by rubella infection were anti-Pr-CA.Chronic cold agglutinin disease is caused by Non-Hodgkin-Lymphomas producing monoclonal CA.
Hemagglutination tests with protease- and neuraminidase(RDE)-treated red
cells are essential to demonstrate anti-Pr cold agglutinins, since RDE and proteases
inactivate the Pr antigens in contrast to the I/i antigens. RDE treatment of red cells,
however, reveals the T antigen which reacts with anti-T present in anti-Pr sera. Furthermore,
anti-I, also present in anti-Pr sera, shows increased reactions with RDE- and proteasetreated
red cells. Therefore, T-anti-T and I-anti-I reactions mask the loss of anti-Pr
activity against RDE- and protease-treated red cells when low-titer anti-Pr sera are studied.
Absorption of anti-Pr sera with RDE-treated red cells removes anti-T and anti-I, leaving
anti-Pr cold agglutinins which only react with untreated red cells, not with RDE- or
protease-treated red cells. Anti-I contaminating anti-Pr in warm eluates from untreated
red cells or stroma can be also removed by absorption with enzyme-treated red cells. By
eliminating T-anti-T interference from sera, it was possible to show that all Pr determinants
known are determined by N-acetylneuraminic acid.
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