Lipid-Modified Antigens

Abstract

Abstract Dodecanoic acid side chains were coupled to the antigen 2,4-dinitrophenyl-bovine serum albumin (DNP-BSA) to make DNP-BSA-lipid. T cells from guinea pigs primed with DNP-BSA-lipid proliferate in vitro when stimulated by most, but not all, DNP-carrier conjugates. Furthermore, DNP-BSA-lipid is a potent stimulator of T cells from DNP-mycobacteria primed animals. This results from its ability to stimulate virtually all DNP-reactive T cells present in such animals, whereas unmodified DNP-BSA stimulates only DNP-BSA reactive clones. When DNP-BSA-lipid was presented to T cells by first absorbing it to peritoneal exudate cells (PEC), it was found that the PEC and the immune T cells had to share I region genes for stimulation to occur. DNP groups can be shown to be present on the surfaces of DNP-BSA-lipid pulsed PEC, as determined by binding of radioactive anti-DNP antibody. Unlabeled anti-DNP will inhibit the binding of labeled anti-DNP to the pulsed PEC, but the presence of the anti-DNP in culture will not prevent stimulation of DNP-reactive T cells by the same pulsed PEC. Taken together, these data suggest that lipid modification of DNP-BSA leads to an increase in its affinity for cell surfaces. Furthermore, they may indicate that this antigen can mimic other DNP-protein antigens by means of a nonspecific association with I region gene products on the surfaces of antigen-presenting cells.