Abstract
Covalent coupling of lipid to protein antigen, BSA, modifies the immunogenicity leading to selective induction of delayed type hypersensitivity in mice with no or very little concomitant antibody production. The mode of linkage of lipid to protein, however, controls its tissue distribution and retention in the body and cell uptake in vitro. Whereas D-BSA accumulates in the draining lymph node after foot pad inoculation, DA-BSA stays at the site. Further, DA-BSA is eliminated much more slowly and D-BSA more quickly from the body than the native antigen. Although both lipid-conjugates are taken up by lymphoid cells in vitro more than the native antigen, DA-BSA binds significantly more than D-BSA. On the basis of in vitro blastogenic response and enumeration of antigen sensitive cells and in vivo tests of delayed type hypersensitivity, DA-BSA appears superior to D-BSA but neither was as potent as BSA in CFA.
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