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: 6 November 2020| Version 1 | DOI: 10.17632/25x7w7hv4y.1
Xiuju Dai


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.



Ehime Daigaku Daigakuin Igakukei Kenkyuka Igakubu


Atopic Dermatitis, Keratinocyte, Interleukin-33