Signals provided in vivo by human rIL-2 and Con A can switch hapten-specific tolerance from unresponsiveness to responsiveness in the South African clawed toad.

Injection in vivo of trinitrobenzene sulphonic acid (TNBS) will conjugate trinitrophenyl (TNP) to the cells and proteins of rodents, and induce hapten-specific tolerance to this epitope. However, the induction of hapten-specific tolerance by this method in the South African clawed toad, Xenopus laevis, is restricted to its subsequent presentation on Ficoll or polyvinylpyrrolidone (PVP). This restricted tolerance depends on the stimulation of an N-methyl-N-nitrosourea (NMU)-insensitive, cyclophosphamide (CyP)-sensitive hapten-specific (suppressor) population that is functionally demonstrable in vitro. Unresponsiveness to TNP-Ficoll can be switched to responsiveness by injection in vivo of recombinant DNA-produced human IL-2 (rIL-2) or the plant-derived lectin, concanavalin A (Con A). Responsiveness to TNP-Ficoll requires thymic presence, although thymic extracts from rIL-2- or Con A-injected toads will suffice. Unresponsiveness to TNP-PVP can also be broken by these reagents, but thymic presence is not required with this immunogen. TNP-Ficoll responses are thymus requiring, while those to TNP-PVP are not, in the toad. Since TNBS failed to stimulate hapten-specific tolerance to a secondary challenge to TNP-Ficoll, we suggest that the suppressor function involved in the establishment of the unresponsive state may act on the differentiation, rather than on the function, of the relevant B cells.