Peripheral blood leukocytes from all normal humans tested have generated trinitrophenyl (TNP)-dependent cytotoxic activity after in vitro sensitization with TNP-modified autologous cells. Weak cytotoxic activity was generated during primary culture; total cytotoxic activity increased approximately 100-fold during secondary stimulation and another 5-fold during tertiary stimulation. The cytotoxic activity was shown to be TNP-dependent at both the sensitization and the lytic phases. Effectors lysed not only TNP-modified autologous cells but all TNP-modified human leukocyte targets tested, including those that shared no serologically defined HLA-A, -B, or -C locus determinants with the specific target. This cross-reactivity was species specific, since it was not observed when human effectors were tested on TNP-modified mouse targets. The TNP-dependent cytotoxic activity on autologous and unrelated cells was shown to be mediated by T cells without requirement for Fc-bearing cells; cytotoxic activity was recovered in subpopulations of cells positively selected by sheep erythrocyte-rosetting techniques and in subpopulations negatively selected by depletion of phagocytic cells, sIg-positive lymphocytes, and Fc-receptor positive lymphocytes. Furthermore, unlike ADCC mediated by anti-TNP antibody, the cytotoxic activity was inhibited by TNP-modified autologous cells, but not by TNP-lysine, or TNP-conjugated chicken red blood cells. We conclude that some human cytotoxic T cells raised against TNP-modified autologous cells because they express a receptor for TNP in conjunction with cell surface determinant(s) that are widely shared among humans but not shared with mice.

This content is only available via PDF.
You do not currently have access to this content.