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Critical Reviews™ in Immunology
インパクトファクター: 1.352 5年インパクトファクター: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN 印刷: 1040-8401
ISSN オンライン: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.2018026335
pages 453-470

IL-33 in Tumor Immunity: Nothing to Sneeze At

Donye Dominguez
Robert H. Lurie Comprehensive Cancer Center, Department of Medicine–Division of Hematology/Oncology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China
Yi Zhang
Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China
Bin Zhang
Robert H. Lurie Comprehensive Cancer Center, Department of Medicine–Division of Hematology/Oncology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China

要約

Although immunotherapy has been at the forefront of cancer therapy for the last several years, better clinical responses are still desired. Interleukin-33 is perhaps one of the most overlooked antitumor cytokines. Its ability to promote type 1 immune responses, which control tumor growth in preclinical animal models is overshadowed by its association with type 2 immunity and poor prognosis in some human cancers. Accumulating evidence shows that IL-33 is a powerful new tool for restoring and enhancing the body's natural antitumor immunity cycle. Furthermore, the antitumor mechanisms of IL-33 are two-fold, as it can directly boost CD8+ T cell function and restore dendritic cell dysfunction in vivo. Mechanistic studies have identified a novel pathway induced by IL-33 and its receptor ST2 in which dendritic cells avoid dysfunction and retain cross-priming abilities in tumor-bearing conditions. Here, we also comment on IL-33 data in human cancers and explore the idea that endogenous IL-33 may not deserve its reputation for promoting tumor growth. In fact, tumors may hijack the IL-33/ST2 axis to avoid immune surveillance and escape antitumor immunity.


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