Chemical reduction of oxidized human lymphocytes inhibits interleukin 2 production but not induction of interleukin 2 responsiveness.
Treatment with neuraminidase (NA) plus galactose oxidase (GalOxase) does not cause stimulation of human thymocytes. However, stimulation can be achieved by addition of exogenous interleukin 2 (IL-2). The IL-2-induced stimulation was inhibited with anti-Tac antibody, indicating that NA/GalOxase-oxidized cells can serve as inducers of functional IL-2 receptors on IL-2-responding T cells. The induction of IL-2 receptors by the oxidized cells was not inhibited by subsequent reduction with borohydride, since the cells could still be stimulated with IL-2. The presence of IL-2 receptors was also confirmed by flow cytometry using indirect immunofluorescence. Peripheral blood lymphocytes can be stimulated by NA/GalOxase treatment, and the conditioned medium from this treatment can support the growth of an IL-2-dependent line. This stimulation can be inhibited with borohydride and restored with IL-2. The conditioned medium derived from the borohydride-reduced cells cannot support the growth of the IL-2-dependent line, indicating that borohydride inhibits the oxidation-induced IL-2 production. The results suggest that NA/GalOxase-oxidized sites can be modified chemically without losing the potential to induce IL-2 receptors.
D002460:Cell Line; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D005692:Galactose Oxidase / Q000494:pharmacology*; D006801:Humans; D007376:Interleukin-2 / Q000096:biosynthesis* / Q000502:physiology; D007700:Kinetics; D008214:Lymphocytes / Q000187:drug effects / Q000276:immunology*; D009439:Neuraminidase / Q000494:pharmacology*; D010084:Oxidation-Reduction
D007376:Interleukin-2; D005692:Galactose Oxidase; D009439:Neuraminidase