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Stromal interleukin-33 promotes regulatory T cell-mediated immunosuppression in head and neck squamous cell carcinoma and correlates with poor prognosis. | LitMetric

AI Article Synopsis

  • Regulatory T cells (Tregs) contribute to immune suppression in head and neck squamous cell carcinoma (HNSCC), and interleukin-33 (IL-33) may enhance Treg proliferation and function in the tumor environment.
  • In a study of 68 laryngeal cancer patients, increased levels of stromal IL-33 were linked to more Treg infiltration and worse patient outcomes as the disease progressed.
  • The research suggests that targeting IL-33 could be a promising approach for immunotherapy in HNSCC due to its role in promoting Treg expansion and activity.

Article Abstract

Regulatory T cells (Tregs) mediate immunosuppressive signals that can contribute to the progression of head and neck squamous cell carcinoma (HNSCC). Interleukin-33 (IL-33) is defined as an 'alarmin', an endogenous factor that is expressed during tissue and cell damage, which has been shown to promote Treg proliferation in non-lymphoid organs. However, the interaction between IL-33 and Tregs in the HNSCC tumor microenvironment remains uncertain. In this study, we examined IL-33 and Foxp3 cells by immunohistochemistry in 68 laryngeal squamous cell cancer patients, followed by functional analysis of IL-33 in Tregs. In addition, the suppressive function of Tregs was assessed by cell proliferation assays. The level of stromal IL-33 was significantly upregulated in advanced versus early stage HNSCC patients and positively correlated with Foxp3 Treg infiltration as well as a poor prognosis. ST2 is regarded as the only receptor of IL-33. Infiltrated ST2-expressing Tregs were responsive to IL-33, and the percentage of Tregs was increased upon IL-33 stimulation. Functional investigation demonstrated that IL-33 increased the proportion of Foxp3GATA3 Tregs and improved the suppressive functions of Tregs by inducing IL-10 and TGF-β1 as well as decreasing the proliferation of responder T cells. Blockade of ST2 abrogated the immunosuppression caused by IL-33. Our data demonstrate that stromal IL-33 both expands the Treg population and enhances their functions in the tumor microenvironment. Furthermore, stromal IL-33 has prognostic value for tumor progression. Thus, stromal IL-33 is a potential target for future HNSCC immunotherapy.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11028137PMC
http://dx.doi.org/10.1007/s00262-018-2265-2DOI Listing

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