FIGURE 3.

Schematic model of T cell proliferation mediated by an IL-2-dependent autocrine mechanism. Stage 1: resting T cells or T cell clones express few or no IL-2 receptors, while reciprocally displaying a maximal number of antigen receptors (V). Stage 2: T3-Ti triggering by antigen/MHC-restricting element or surface bound anti-T cell receptor antibodies results in T3-Ti modulation, thus reducing the number of surface antigen receptors and rapidly inducing surface IL-2 receptor expression. Stage 3: This event appears to occur prior to IL-2 secretion itself because IL-2 receptor expression can be observed 2–4 h after T3-Ti triggering, whereas IL-2 is not detectable in culture supernatants until at least 10–12 h later. Stage 3 can also be achieved with anti-Ti or anti-T3 monoclonal antibodies in soluble form. Stage 4: activation via Ti-T3 leads to production and secretion of endogenous IL-2 (•) and subsequent binding to its own IL-2 receptors. Stage 5: once a critical density of occupied IL-2 receptors is achieved, DNA synthesis and mitosis occur. Finally, in the absence of additional antigenic stimulation, there is re-expression of the surface T3-Ti complex (stage 1). Redrawn from Meuer et al. (1984).