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.