title: Impaired T cell functions during amphibian metamorphosis: IL-2 receptor expression and endogenous ligand production.
abstract: T cell functions are impaired during defined developmental stages of amphibian metamorphosis (Marx et al., 1987). Here we show, using a fluorescent anti-human IL-2 receptor antibody and flow cytometry, that during these stages, the splenocytes of Xenopus laevis, the South African clawed toad, have a progressively diminished capacity to express IL-2 receptors (IL-2R), after in vitro lectin stimulation. Preincubation with human rIL-2 specifically blocks binding of the anti-IL-2R antibody. Separation of an endogenous ligand bound to the IL-2R leads to a substantial increase in available epitope recognized by the anti-IL-2R antibody when pre- and postmetamorphic splenocytes are employed, but not when splenocytes of the prometamorphic stages are treated similarly. Thus, the cells from the prometamorphic stages are not producing significant quantities of the ligand. Finally, we demonstrate that human rIL-2 is not by itself mitogenic in the toad, but it can act as a co-stimulator of antigen-induced mitogenesis. Thus, an absence of an endogenous ligand (autologous IL-2?), coupled with a reduced capacity to express IL-2 receptors may be responsible for impaired T cell clonal expansion in metamorphosing Xenopus. Inhibition of T cell functions during this period is vital, since adult cells forming within the larval body bear surface proteins not found on larval cells (Flajnik et al., 1986).
authors.affiliation: Biology Department, Reed College, Portland, OR 97202-8199.
authors.forename: L N
authors.initials: LN
authors.lastname: Ruben
authors.forename: M A
authors.initials: MA
authors.lastname: Scheinman
authors.forename: R O
authors.initials: RO
authors.lastname: Johnson
authors.forename: S
authors.initials: S
authors.lastname: Shiigi
authors.forename: R H
authors.initials: RH
authors.lastname: Clothier
authors.forename: M
authors.initials: M
authors.lastname: Balls
mesh_terms: D000818:Animals; D016923:Cell Death; D003345:Corticosterone / Q000097:blood; D006801:Humans; D007108:Immune Tolerance; D007111:Immunity, Cellular; D007376:Interleukin-2 / Q000494:pharmacology; D008024:Ligands; D008675:Metamorphosis, Biological / Q000276:immunology*; D015375:Receptors, Interleukin-2 / Q000096:biosynthesis*; D011994:Recombinant Proteins / Q000494:pharmacology; D013601:T-Lymphocytes / Q000276:immunology*; D014982:Xenopus laevis / Q000254:growth & development* / Q000276:immunology
chemical_list: D007376:Interleukin-2; D008024:Ligands; D015375:Receptors, Interleukin-2; D011994:Recombinant Proteins; D003345:Corticosterone