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IL-33 Released in the Liver Inhibits Tumor Growth via Promotion of CD4 + and CD8 + T Cell Responses in Hepatocellular Carcinoma

The Journal of immunology (1950), 2018-12, Vol.201 (12), p.3770-3779 [Peer Reviewed Journal]

Copyright © 2018 by The American Association of Immunologists, Inc. ;ISSN: 0022-1767 ;EISSN: 1550-6606 ;DOI: 10.4049/jimmunol.1800627 ;PMID: 30446569

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  • Title:
    IL-33 Released in the Liver Inhibits Tumor Growth via Promotion of CD4 + and CD8 + T Cell Responses in Hepatocellular Carcinoma
  • Author: Jin, Ziqi ; Lei, Lei ; Lin, Dandan ; Liu, Yonghao ; Song, Yuan ; Gong, Huanle ; Zhu, Ying ; Mei, Yu ; Hu, Bo ; Wu, Yan ; Zhang, Guangbo ; Liu, Haiyan
  • Is Part Of: The Journal of immunology (1950), 2018-12, Vol.201 (12), p.3770-3779
  • Description: IL-33 released by epithelial cells and immune cells functions as an alarmin and can induce both type 1 and type 2 immune responses. However, the role of IL-33 release in tumor development is still not clear. In this study, we examined the function of released IL-33 in murine hepatocellular carcinoma (HCC) models by hydrodynamically injecting either IL-33-expressing tumor cells or IL-33-expressing plasmids into the liver of tumor-bearing mice. Tumor growth was greatly inhibited by IL-33 release. This antitumor effect of IL-33 was dependent on suppression of tumorigenicity 2 (ST2) because it was diminished in ST2 mice. Moreover, HCC patients with high IL-33 expression have prolonged overall survival compared with the patients with low IL-33 expression. Further study showed that there were increased percentages and numbers of activated and effector CD4 and CD8 T cells in both spleen and liver in IL-33-expressing tumor-bearing mice. Moreover, IFN-γ production of the CD4 and CD8 T cells was upregulated in both spleen and liver by IL-33. The cytotoxicity of CTLs from IL-33-expressing mice was also enhanced. In vitro rIL-33 treatment could preferentially expand CD8 T cells and promote CD4 and CD8 T cell activation and IFN-γ production. Depletion of CD4 and CD8 T cells diminished the antitumor activity of IL-33, suggesting that the antitumor function of released IL-33 was mediated by both CD4 and CD8 T cells. Taken together, we demonstrated in murine HCC models that IL-33 release could inhibit tumor development through its interaction with ST2 to promote antitumor CD4 and CD8 T cell responses.
  • Publisher: United States
  • Language: English
  • Identifier: ISSN: 0022-1767
    EISSN: 1550-6606
    DOI: 10.4049/jimmunol.1800627
    PMID: 30446569
  • Source: GFMER Free Medical Journals
    Alma/SFX Local Collection
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