The dual role of interleukin 1 in lectin-induced proliferation of T cells.

Nylon wool non-adherent, thoroughly macrophage-depleted rat thymocytes (NaTs) or lymph node cells (NALs) pulsed with Con A for 20 h did not proliferate and acquired a very low level of IL 2 responsiveness or were completely unresponsive to exogenous IL 2. When supplemented with irradiated resident peritoneal cells used as a source of macrophages during Con A pulsing, NATs/NALs became capable of proliferating and expressing competence to respond to exogenous IL 2. Thus in the experimental system used in this study both IL 2 production and acquisition of IL 2 responsiveness are macrophage-dependent. Semipurified rat IL 1 could efficiently replace the requirement for macrophages in the promotion of proliferation of NATs/NALs both in the presence or absence of exogenous IL 2. Furthermore, NATs/NALs pretreated with IL 1 for 6 h before Con A pulsing were able to acquire reactivity to IL 2. The effect of IL 1 pretreatment in promoting the Con A-induced IL 2 responsiveness of NATs/NALs was dose-dependent. IL 1 by itself did not induce competence to IL 2. IL 1 pretreatment did not alter the overall Con A-binding capacity of NATs nor the ability of Con A to aggregate them. Irradiated IL 1-pretreated NATs could not accomplish the function of "accessory cells" for induction of IL 2 responsiveness of untreated NATs by Con A. Our study indicates that IL 1 exerts two activities in lectin-induced proliferation of at least some resting T cells present both in thymus and lymph nodes. On the one hand, IL 1 promotes IL 2 production and, on the other hand, it promotes expression of IL 2 receptors.