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. 2015 Jul 27;195(5):2353–2364. doi: 10.4049/jimmunol.1500300

FIGURE 5.

FIGURE 5.

Effect of lymphocyte depletion on IL-15 SA–induced toxicity. Mice were treated with 2 μg IL-15 SA for 4 d; rectal temperature was measured on day 5. (A) Mice were treated with anti-asialoGM1 or anti-NK1.1 IgG to deplete NK and NKT cells 1 d before initiation of 2 μg IL-15 SA treatment. (B) Serum AST and ALT concentrations in mice treated with anti-NK1.1 or nonspecific IgG were measured at 24 h after the fourth i.p. injection of 2 μg IL-15 SA. Vehicle-treated mice served as control. (C) CD1d KO mice were treated with 2 μg IL-15 SA. (D) CD8 T cells were depleted by treatment with anti-CD8α IgG at 24 h prior to IL-15 SA treatment or CD8 KO mice were treated with IL-15 SA. (E) Serum AST and ALT levels in mice treated with anti-CD8α IgG or nonspecific IgG were measured at 24 h after the last injection of IL-15 SA. (F) To deplete NK and NKT cells in CD8 KO mice, CD8 KO mice were treated with anti-asialoGM1 1 d before IL-15 SA treatment. Isotype-specific or nonspecific IgG served as control in Ab-induced leukocyte depletion experiments. WT mice served as control for experiments using genetically altered mice. NK (G and J), NKT (H and K), and mCD8+ T cells (I and L) from spleens of WT mice were characterized in mice treated with anti-asiaoGM1, anti-NK1.1, or anti-CD8α IgG as well as in CD8 KO mice. Untreated WT mice or WT mice treated with isotype matched IgG served as controls. n = 6–10 mice/group. Data are representative of two to three separate experiments. *p < 0.05 compared with untreated WT control, +p < 0.05 compared with IgG group or WT control, #p < 0.05 compared to CD8KO treated with IgG.