Interleukin-2-induced mortality during the metamorphosis of Xenopus laevis.

In anuran metamorphosis, histoincompatible adult cells arise within an immunocompetent larval body. However, the larvae are unresponsive to these altered-self cells. The basis for this tolerance is an issue of considerable interest. While a loss of tolerance in mammalian pregnancy may initiate localized abortion, since the entire metamorphic amphibian is involved, there is the potential for total body self-destruction. Metamorphosing Xenopus laevis, the South African clawed toad, produce an internal corticosterone environment that induces T-cell anergy. This impairment may save the animal from immune self-destruction. Here we examine the capacity of recombinant gene produced human interleukin 2 (IL-2) to substitute for, or restore the level of autologous IL-2, as a further test of whether the altered-self tolerance found during metamorphosis may rely on corticosteroid-induced anergy. We find that the capacity of rIL-2 to break this tolerance and stimulate mortality is low, unless it is accompanied by antigenic co-stimulation. A study of sections of experimental and control animals revealed lymphocyte and mast cell increases within the kidney, particularly in the region of the coelomoduct, perhaps reflecting autoimmune reactivity responsible for the mortality.