Abstract
Abstract An NZB-derived IgG2a myeloma protein with anti-dinitrophenol (DNP) activity was assayed for its ability to elicit complement fixation (CF) and passive cutaneous anaphylaxis (PCA) in guinea pigs after it had been combined with DNP antigens. The myeloma protein agglutinates difluorodinitrobenzene-coupled red cells and this agglutination can be inhibited by monovalent DNP amino acids, albeit with approximately 1000-fold more inhibitor than that needed to inhibit agglutination by a mouse anti-DNP serum. Despite the ability to agglutinate DNP red cells, no passive hemolysis occurred. The myeloma protein gave reverse PCA reactions in guinea pig skin with as little as 0.12 μg and challenge by anti-mouse globulin. However, even with 40 μg per skin site, no PCA reactions could be elicited on challenge with DNP conjugates. It is concluded that the complete biologically active sites on IgG2a molecules for CF and PCA reactions are created by the energy of binding of the molecule to its antigen. The myeloma anti-DNP protein does not create these sites after antigen binding because of its extremely low affinity.
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