Figure 7.
Intestinal organoids derived from ATG16L1T300Ahomozygous individuals exhibit heightened susceptibility to TNF-α and allogeneic T cells. (A) Proportion of human small intestinal organoids from Figure 6B and 6C that were susceptible (displayed >50% lethality) to recombinant TNF-α (left panel) or allogeneic T cells (right panel). n = 14 (nonrisk) and n = 6 (T300A/T300A). Statistical significance was validated with Fisher’s exact test. (B) Combined organoid viability in A; n = 14 (nonrisk) and n = 6 (T300A/T300A). Data points represent an average viability of individual organoids in Figure 6. Representative images (C) and viability (D) of human small intestinal organoids stimulated or not with 50 ng/mL TNF-α, 100 nM ruxolitinib, 1 μM GSK547, 20 μM necrostatin-1s (Nec-1s), or 2 μM necrosulfonamide (NSA) for 48 hours. Scale bars, 400 µm. Data points are mean of technical replicates. At least 2 independent experiments were performed. ***P < .001, ****P < .0001.

Intestinal organoids derived from ATG16L1T300Ahomozygous individuals exhibit heightened susceptibility to TNF-α and allogeneic T cells. (A) Proportion of human small intestinal organoids from Figure 6B and 6C that were susceptible (displayed >50% lethality) to recombinant TNF-α (left panel) or allogeneic T cells (right panel). n = 14 (nonrisk) and n = 6 (T300A/T300A). Statistical significance was validated with Fisher’s exact test. (B) Combined organoid viability in A; n = 14 (nonrisk) and n = 6 (T300A/T300A). Data points represent an average viability of individual organoids in Figure 6. Representative images (C) and viability (D) of human small intestinal organoids stimulated or not with 50 ng/mL TNF-α, 100 nM ruxolitinib, 1 μM GSK547, 20 μM necrostatin-1s (Nec-1s), or 2 μM necrosulfonamide (NSA) for 48 hours. Scale bars, 400 µm. Data points are mean of technical replicates. At least 2 independent experiments were performed. ***P < .001, ****P < .0001.

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