Adult induccr T cells are activated by foreign antigens in the context of learned self major hislocompatibility complex (MHC) molecules, but are unresponsive (tolerant) to most sell antigens (reviewed in Schwartz 1984). Recently, our knowledge of T-cell activation has been greatly extended by discoveries concerning the molecular structures of the T-cell receptor (reviewed in Kronenberg et al. 1986) and MHC molecules (reviewed in Germain & Malissen 1986). the role of lymphokines in T-cell proliferatioti and differentiation (reviewed in Smith 1984), and the biochemical events resulting from T-cell receptor occupancy (reviewed in Weiss et al. 1986). In contrast, very little is known about the cellular and molecular mechanisms underlying the induction of T-cell tolerance. Experimentally, T-cell unresponsiveness can be induced in neonates by injection of soluble or particulate antigen, or in adults by the intravenous injection of high doses of soluble antigen or of antigen coupled to syngeneic spleen cells (Borel 1980, Claman et al. 1980, Ramos et at. 1980, Germain & Benacerraf 198K Nossal 1983, Monroe et al. 1984. Oki & Sercarz 1985). These studies have provided evidence for two models of tolerance:

1) indirect inhibition of inducer T cells by suppressor T cells 2) direct inactivation of inducer T cells by antigen. In the suppression model, a complex circuit of interacting suppressor T cells