The expression of interleukin 2 (IL-2), induction of its multisubunit receptor and subsequent interplay of this ligand with its receptor are pivotal events in T-cell activation. Our present understanding of the normal IL-2flL-2R system and of disorders in this network in disease opens the possibility for more specific immune intervention. Thomas Waldmann discusses the clinical application of IL-2, agents that inbibit IL-2 synthesis and action, and how the anti-IL-2 receptor-directed therapy provides a novel perspective for prevention of allograft rejection and for treatment of graft versus host disease, select autoimmune disorders and certain neoplastic diseases.

The body defends itself against foreign invaders by a defense system involving antibodies and thymusderived lymphocytes (T cells). To mediate immune responses, T cells must change from a resting to an activated state. T cells stimulated by foreign antigens enter a program of cellular activation leading to de novo synthesis of interleukin 2 (IL-2) 1-3 (Fig. 1). Resting T cells do not express high affinity receptors (IL-2Rs) but these are rapidly expressed after activation 2'4. Interaction of IL-2 with its induced cellular receptors triggers cellular proliferation culminating in the emergence of effector T cells that are required for the full expression of immune responses,