IL-33 in Tumor Immunity: Nothing to Sneeze At

D Dominguez, Y Zhang, B Zhang

Research output: Contribution to journalArticle

5 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)453-470
Number of pages18
JournalCritical reviews in immunology
Issue number6
StatePublished - 2018

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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