Corticosteroid regulation of IL-1 production may be responsible for deficient immune suppressor function during the metamorphosis of Xenopus laevis, the South African clawed toad.

Thymus immune suppressor function is deficient during the metamorphosis of Xenopus laevis, the South African clawed toad. Thymuses of antigen-activated metamorphic larvae were tested for restoration of suppressor function by co-culture with matched fragments of spleens from immunized, antibody-producing young adults. The inhibition of unusually high endogenous corticosteroid levels in metamorphic larvae with metyrapone restores suppressor function. Dexamethasone counteracts this effect. Since corticosteroids can inhibit clonal expansion of thymus-derived (T) immunocytes by effecting lymphokines in mammals, we tested recombinant DNA-produced human interleukin-1 (rIL-1) and interleukin-2 (rIL-2), and the lectin concanavalin A in vivo. All restore thymus suppressor function in metamorphosing larvae. When metyrapone, dexamethasone and rIL-2 are injected together into antigen-activated larvae their thymuses will suppress splenic antibody production. Moreover, since rIL-1 and rIL-2 are able to restore thymic suppression in antigen-activated metamorphic larvae, endogenous corticosteroid does not effect their function. The basis for the lack of suppressor function during metamorphosis of Xenopus laevis may be endogenous corticosteroid regulation of IL-1 production to create IL-2 deficiency, thereby inhibiting T cell clonal expansion.