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The journal of immunology : official journal of the American Association of Immunologists v.198 no.3, 2017년, pp.1365 - 1375   SCI SCIE
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Exogenous IL-33 Restores Dendritic Cell Activation and Maturation in Established Cancer

Dominguez, Donye (Division of Hematology/Oncology, Robert H. Lurie Comprehensive Cancer Center, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611 ) ; Ye, Cong (Division of Hematology/Oncology, Robert H. Lurie Comprehensive Cancer Center, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611 ) ; Geng, Zhe (Division of Hematology/Oncology, Robert H. Lurie Comprehensive Cancer Center, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611 ) ; Chen, Siqi (Division of Hematology/Oncology, Robert H. Lurie Comprehensive Cancer Center, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611 ) ; Fan, Jie (Division of Hematology/Oncology, Robert H. Lurie Comprehensive Cancer Center, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611 ) ; Qin, Lei (Division of Hematology/Oncology, Robert H. Lurie Comprehensive Cancer Center, Department of Medicine, Northwestern Unive ) ; Long, Alan ; Wang, Long ; Zhang, Zhuoli ; Zhang, Yi ; Fang, Deyu ; Kuzel, Timothy M. ; Zhang, Bin ;
  • 초록  

    The role of IL-33, particularly in tumor growth and tumor immunity, remains ill-defined. We show that exogenous IL-33 can induce robust antitumor effect through a CD8 + T cell–dependent mechanism. Systemic administration of rIL-33 alone was sufficient to inhibit growth of established tumors in transplant and de novo melanoma tumorigenesis models. Notably, in addition to a direct action on CD8 + T cell expansion and IFN-γ production, rIL-33 therapy activated myeloid dendritic cells (mDCs) in tumor-bearing mice, restored antitumor T cell activity, and increased Ag cross-presentation within the tumor microenvironment. Furthermore, combination therapy consisting of rIL-33 and agonistic anti-CD40 Abs demonstrated synergistic antitumor activity. Specifically, MyD88, an essential component of the IL-33 signaling pathway, was required for the IL-33–mediated increase in mDC number and upregulation in expression of costimulatory molecules. Importantly, we identified that the IL-33 receptor ST2, MyD88, and STAT1 cooperate to induce costimulatory molecule expression on mDCs in response to rIL-33. Thus, our study revealed a novel IL-33–ST2–MyD88–STAT1 axis that restores mDC activation and maturation in established cancer and, thereby, the magnitude of antitumor immune responses, suggesting a potential use of rIL-33 as a new immunotherapy option to treat established cancer.


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