Nuclear IL-33 plays an important role in the suppression of filaggrin, loricrin, keratin 1, and keratin 10 by IL-4 and IL-13 in human keratinocytes

Published: 06-11-2020| Version 1 | DOI: 10.17632/25x7w7hv4y.1
Contributor:
Xiuju Dai

Description

The data in Fig. 1 showed that IL-4/IL-13 increases IL-33 expression in the nucleus by activating ERK (not STAT3 and STAT6) signaling pathway. The data in Fig. 2 showed that nuclear IL-33 is involved in the downregulation of differentiation markers. The data in Fig. 3 showed that Nuclear IL-33 contributes to the downregulation of FLG, LOR, KRT1, and KRT10 by regulating the nuclear translocation of STAT3 and STAT6 The data in Fig. 4 showed that Nuclear IL-33 functions as a transcription cofactor of STAT3, facilitating p-STAT3 to the FLG promoter thereby inhibiting FLG transcription. The data in Fig. 5 showed that IL-4/IL-13 decreases the expression of RunX1 through activating STAT3 and STAT6. The data in Fig. 6 showed that Nuclear IL-33 participates in the downregulation of LOR, KRT1, and KRT10 by reducing the RunX1 level. The data in Fig. S1 showed that Both IL-4 and IL-13 increase IL-33 expression, which is required for the downregulation of FLG, LOR, KRT1, and KRT10. The data in Fig. S2 showed that Cytokine IL-33 is not involved in the downregulation of FLG by IL-4/IL-13. The data in Fig. S3 showed that IL-4/IL-13 upregulates IL-33 by increasing its protein stability. The data in Fig. S4 showed that IL-33 knockdown regulates the phosphorylation of ERK, STAT3, and STAT6 in NHEKs; and siRNA transfection causes IL-33 cleavage. The data in Fig. S5 showed that STAT3-binding sites in the FLG promoter and PCR primers for ChIP assay were presented; the knockdown of IL-33 by IL-33 siRNA and the inactivation of STAT3 by AxSTAT3F regarding ChIP-samples were confirmed. Table S1 showed the primary antibodies and their dilution used for WB, IHC, IF, and ChIP in this study.

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