Abstract
As compared with the native molecule, recombinant human interleukin-2 that is modified by covalently attached polyethylene glycol residues (IL-2-PEG) exhibits a markedly enhanced half-lifein vivo, thus facilitating its biological evaluation. We have characterized the effect of IL-2-PEG on theStaphylococcus aureusenterotoxin B (SEB)-induced tolerance of peripheral SEB-reactive (Vβ8+) T cells. Treatment with sublethal doses of IL-2-PEG does not modulate (inhibit or enhance) the SEB-triggered apoptosis and deletion of Vβ8+T cells. In contrast,in vivotreatment with IL-2-PEG partially abolishes the SEB-triggered anergy of Vβ8+T cells, i.e., the failure to proliferate in response to SEBin vitro. To abolish SEB-triggered anergy, IL-2-PEG must act for an extended periodin vivo; short term treatmentin vivo(2 days) or exposure of anergic T cells to IL-2in vitrofails to reconstitute proliferative responses. Moreover, the effect ofin vivotreatment with IL-2-PEG on lymphokine production by anergic T cells is partial. IL-2-PEG restores IL-4-dependent autocrine proliferation in response to SEB but does not reestablish defective IL-2 production. These data are compatible with the notion that IL-2 is a regulator of postdeletional rather than deletional T cell tolerance.
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