One of the main problems confronting an immune system designed to eliminate foreign substances is the establishment and maintenance of self tolerance. Two schools of thought exist on how self-reactivity in the T cell compartment is avoided. One mechanism, clonal deletion, proposes that self-tolerance is imposed on immature T cells in the thymus-that at a certain stage of differentiation, contact with antigen permanently inac tivates the cell (1, 2). An alternative, nonmutually exclusive suggestion is that anti-idiotypic suppressor mechanisms exist to inhibit continually any potential self reactivity. According to this hypothesis, anti-A reactive T cells are held in check by anti-(anti-A) suppressor T cells (3, 4, 5). Most self-tolerance in the population of T cells is apparently imposed by clonal deletion of auto reactive lymphocytes within the thymus. However, this mechanism of avoiding autoimmune recognition may alone be insufficient, as auto reactive T cells can be isolated from the population of mature peripheral lymphocytes, and in fact, syngeneic cytolysis can be demon strated in many allospecific cytotoxic T lymphocyte (C TL) clones (6). In the following pages we argue for the presence of a mechanism, other than one involving anti-idiotypic networks, for the continued maintenance of self-tolerance in the pool of peripheral lymphocytes. This form of antigen-specific suppression results in the functional elimination of auto reactive peripheral T cells by other lymphoid cells, the most effective being