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W G Graven

Publications and source records attributed to W G Graven.

2 recordsLinked to original sources
PubMed1975

Antibody formation in the mouse induced by hapten-carrier complexes.

The influence of hapten, carrier and their ratio in a complex on T-cell helper stimulation and antibody formation against the dinitrophenyl (DNP) hapten was studied. Complexes of DNP with bovine serum albumin (BSA), bovine gamma-globulin (BGG), isologous mouse immunoglobulin (MIG) and polyvinylpyrrolidone (PVP) as carriers were used. Optimal antibody formation against DNP was obtained with complexes with an intermediate hapten:carrier ratio (DNP 16-minusBSA, DNP 43-minusBGG and DNP 48-MINUSMIG). DNP-PVP complexes were not active either in the primary or in the secondary response. The anti-BSA titre was independent of the number of DNP groups on the complex used for immunization. Inhibition of DNP-plaque formation by spleen cells of immunized mice shows an increase of the inhibitory capacity of the complex with the increase of the hapten-carrier ratio. DNP 16-minusPVP was the only PVP complex which was inhibitory. These results suggest that helper cells involved in the antibody formation against BSA and DNP are reactive with different parts of the complex. Priming of mice with carrier or complex after cyclophosphamide (Cy) treatment followed by a secondary injection with complex 10 days later gave strong indications that there is a greater involvement in stimulation of helper T cells by determinants of the complex (new antigenic determinants (NAD) or NAP-DNP groups) or DNP, than by true BSA determinants. This holds for both the IgM and IgG responses.

Animals↗
PubMed1975

Delayed hypersensitivity in the mouse induced by hapten-carrier complexes.

Delayed hypersensitivity (DH) in the mouse was studied with complexes of dinitrophenyl (DHP) as hapten and bovine serum albumin (BSA), mouse immunoglobulin (MIg) and polyvinylpyrrolidone (PVP) as carrier. Priming with BSA induced strong DH against this carrier, but DN of decreasing strength against complexes with increasing DNP:carrier ratio. Priming with DNP-BSA complexes never resulted in a DH against BSA or DNP 3-minusBSA. Injections of DNP 16-minusBSA and DNP 28-minusBSA induced positive DH which increased with the hapten:carrier ratio of the eliciting antigen. The complexes with an isologous carrier DNP 48-minusMIg or DNP 90-minusMIg induced positive reactions against both complexes but not against the weakly substituted DNP 11-minusMIg. The latter only primed for itself. The importance of the DNP groups as determinant in these DH reactions is stressed by the cross-reactions between DNP-BSA and DNP-MIg complexes and by the induction by DNP 16-minusPVP of positive DH against DNP 28-minusBSA. Cyclophosphamide (Cy) treatment before priming with complexes induced enhanced DH against complexes with sufficient hapten:carrier ratio. Priming with carrier under Cy treatment induced no DH against complexes. All these results indicate that carrier determinants are not involved in the DH against complexes. After priming wtih complexes with a low hapten:carrier ratio the DH is directed against new antigenic determinants (NAD) groups. After priming with complexes with high ratios DH is directed against DNP groups. With adoptive local transfer of spleen cells of primed animals and pretreatment of these cells with anti-thymocyte serum or anti-plasma cell serum and complement it was possible to demonstrate that the T cell was responsible for the DH reactions. The involvement of different determinant groups on the hapten-carrier complexes in immune reactions is discussed.

Animals↗