If it were possible to promote or suspend the formation of specifically sensitized lymphocytes (activated T cells), the problems of achieving a sustained attack on tumor cells and microbial parasites, or of preventing graft rejection, might be largely overcome. Methods for manipulating the immune response for such purposes have been proposed from time to time (1-3), but progress has been slow because so little is known of how cell-mediated immunity is normally regulated. Although much has been learned about the allied problem cf what controls the formation of antibodies (4), almost nothing is known about the mechanism that regulates the production and function of the cells which mediate delayed-type hypersensitivity (DTH).I While studying the tumor-suppressive activity of Mycobacterium boris BCG it was observed that lymphoid tissues which were under the stimtflatory influence of a BCG infection were capable of a much more vigorous response to a second antigen (5). Both cellular and humoral immunity to sheep red blood cells (SRBC) were augmented, as evidenced by higher and more sustained levels (DTH) and increased numbers of plaque-forming cells (PFC) in responding lymph nodes. Since D T H does not usually appear unless special conditions of immunization are used, these findings suggested that the formation of activated T cells is normally restricted by an inhibitory mechanism that does not operate properly in lymphoid tissues infected with BCG.Miller et al. (5) have shown that mice given a subcutaneous injection of SRBC in saline develop a poorly sustained state of hypersensitivity which conforms to all of the established criteria by which D T H is recognized, including its mediation by 0-bearing lymphocytes. It was therefore possible to study the mechanism which regulates T-cell activity in the absence of any influence from adjuvants such as were used by Nelson and Mildenhall (6) when they, too, showed that mice develop classical D T H in response to SRBC.