ANALYSIS OF ACCESSORY SIGNALING IN HUMAN T-CELL CLONES

Human T cells, when activated, express small but detectable levels of MHC class II on their surface and as a result have the potential to pr esent antigens in the context of MHC class II molecules. There are rep orts demonstrating MHC class II restricted antigen presentation by hum an T-cell clones. In this report, we show evidence for one such clone that can present peptide antigen to itself. This clone, HA1.7m1, is cl early different in its accessory signaling requirements from the paren tal clone HA1.7, and shows a decrease in the surface level of CD54. We have analyzed the accessory signaling abilities of T cells by using H A 1.7m1 as a responder population, and demonstrate that the accessory signaling potential of T-cell clones is sufficient to bring about acti vation of HA1.7m1 but not of HA1.7. This accessory signaling ability i s, however, different from that of B cells in providing bystander acce ssory signals. T-cell APCs cannot provide bystander accessory signals for the proliferative response of HA1.7m1, nor can they block the indu ction of tolerance in this subline, whereas bystander B cells can medi ate both events to a limited extent. Thus, there are significant diffe rences in the accessory signaling abilities of T cells as APCs as comp ared with classic APCs such as B cells, independent of their ability t o generate peptide-MHC complexes. It also appears that although HA1.7m 1 can be activated by self-presentation of antigen, it is still suscep tible to the induction of tolerance. These results may be of relevance in predicting the outcome in terms of T-cell activation and/or tolera nce due to T cells functioning as APCs in the induction and regulation of immune responses in infectious diseases or in peptide-based vaccin ation strategies.