Fig. 5.

CD45 governs the dependence on caspases for cell death signaling via wild-type Gal3, Pentamer, and Hexamer. (A) Percentage of Jurkat T cell apoptosis after 18 h treatment with synthetic Gal3 oligomers or wild-type Gal3 (WT-Gal3) relative to PBS-treated cells (untreated) while in the presence or absence of a pancaspase inhibitor. (B) Percentage of J45.01 T cell apoptosis after 18 h treatment with synthetic Gal3 oligomers or WT-Gal3 relative to untreated cells while in the presence or absence of a pancaspase inhibitor. (C) Percentage decrease in Jurkat and J45.01 T cell apoptosis after caspase inhibition from data in A and B. For A and B, n ≥ 3, mean ± SD, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, NS is no significant difference, and comparisons were made using unpaired two-tailed Student’s t test. For C, n ≥ 3, mean ± SD, *P < 0.05, **P < 0.01, NS is no significant difference, and comparisons were made using one-way ANOVA with Tukey’s post hoc. Statistical comparisons relative to WT-Gal3-treated Jurkat or J45.01 T cells are denoted by * or NS symbol directly above bars, and one outlier (black circle) was detected using Grubbs’ test while removed from mean ± SD calculation. All experiments were performed at an equimolar concentration of sfGFP or Gal3 = 5 µM (i.e., [WT-Gal3] = 5 µM, [Pentamer] = 1 µM, [Hexamer] = 0.83 µM).