Figure 8.

Autosecretory proteins are responsible for autophagy-modulated psoriasis-like skin inflammation in keratinocytes. (A and B) Krt14^+/+-Atg5^f/f and Krt14^Cre/+-atg5^f/f primary murine keratinocytes were stimulated with or without M5 for 24 h in the absence or presence of anti-HMGB1 IgY antibodies (10 μg/mL), anti-IL1B IgG antibodies (10 μg/mL), and anti-IL18 IgG2a antibodies (10 μg/mL); nonimmune IgY, nonimmune IgG or IgG2a were used controls. The indicated genes expression levels were assayed by qRT-PCR. n = 3/group. (C and D) Krt14^+/+-Atg5^f/f and Krt14^Cre/+-atg5^f/f primary murine keratinocytes were stimulated with M5 in the absence or presence of rHMGB1 (10 μg/mL), rIL1B (10 ng/mL), rIL18 (100 ng/mL). The indicated genes expression levels were assayed by qRT-PCR. n = 3/group. (E-G) IMQ was applied daily to Krt14^+/+-Atg5^f/f and Krt14^Cre/+-atg5^f/f mice that were received a daily intradermal injection of rHMGB1 (1 µg), rIL1B (20 ng), and rIL18 (20 ng) for 5 d, n = 5/group. (E) H&E staining skin sections, left: Representative H&E staining data; right: statistical data, scale bar: 100 μm. (F) FACS for IL17A-producing T cells in the back skin. qRT-PCR analysis of the indicated genes from back skin RNA (G). Mean ± SD. *P < 0.05; **P < 0.01; ***P < 0.001; NS, not significant. One-way ANOVA (A-G). All the data are representative of three independent experiments