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 df tolerance in mammalian pregnanc y may initiate localized abortion, since the entire metamorphic amphib ian is involved, there is the potential for total body self-destructio n. Metamorphosing Xenopus laevis, the South African clawed toad, produ ce 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 interleuki n 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 an d mast cell increases within the kidney, particularly in the region of the coelomoduct, perhaps reflecting autoimmune reactivity responsible for the mortality.