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. 2000 Feb 15;105(4):459–468. doi: 10.1172/JCI8185

Figure 1.

Figure 1

Cytotoxic activity of 4.1-CD4+ CTL. (a) PMA and ionomycin–treated and untreated 4.1-CD4+ T cells, propagated from pancreatic islets of acutely diabetic 4.1-NOD mice, were tested for cytotoxic activity against NOD and B6 islet cells (i.c.) (left) and L1210-Fas+ and L1210-Fas– fibroblasts (right). (b) Cytotoxic activity of serine esterase–positive 4.1-CD4+ CTL and 8.3-CD8+ CTL clones against NOD and B6 islet cells at a 1:5 target-to-effector (T:E) ratio. (c) Cytolytic activity of a representative 4.1-CD4+ CTL clone against L1210-Fas+ and L1210-Fas– cells at a 1:5 T:E ratio. (d) and (e) Cytolytic activity of in vitro–differentiated 4.1-CD4+ CTL against NOD (d) or NOD.lpr+/+ (e) islet cells cultured overnight in the absence (0) or presence of IFN-γ (250 U/mL) or IL-1α (100 U/mL) at a 1:10 T:E ratio. Although overnight IL-1α treatment caused a significant reduction in islet yield, the spontaneous chromium release by the surviving islet cells was similar to that by untreated or IFN-γ–treated islet cells (< 35%). (f) Cytolytic activity of 4.1-CD4+ CTL against cytokine-treated NOD islet cells (250 U/mL IFN-γ, 100 U/mL IL-1α, or 250 U/mL IFN-γ + 10 U/mL IL-1α) in the presence of blocking concentrations of anti–MHC class II and class I mAbs (at a 1:10 T:E ratio). (g) Cytolytic activity of 4.1-CD4+ CTL against IFN-γ–(250 U/mL) and IL-1α–treated (10 U/mL) NOD islet cells in the presence of a caspase inhibitor (CI) or a control inhibitor (granzyme B inhibitor; GBI). (h) Cytolytic activity of 4.1-CD4+ CTL against cytokine-treated NOD islet cells (250 U/mL IFN-γ, 100 U/mL IL-1α, 100 U/mL IL-1β, or 250 U/mL IFN-γ + 10 U/mL IL-1α or IL-1β). The figures are representative of 2–3 different experiments (mean ± SEM). Iono, ionomycin.