IL-33 drives the antitumour effects of dendritic cells via upregulating CYLD expression in pulmonary adenocarcinoma.

Lung adenocarcinoma is one of the leading causes of cancer-related death worldwide. Low expression of Interleukin-33 (IL-33) was reported to be associated with the progression of pulmonary adenocarcinoma. However, the IL-33-mediated immunoregulation in pulmonary adenocarcinoma remains unclear. In this study, we found that IL-33 treatment evidently repressed tumour growth, induced CD4⁺ T cells infiltration and IL-17 expression in pulmonary adenocarcinoma. Notably, IL-33 treatment increased the number of Dendritic Cells (DCs) in pulmonary adenocarcinoma. More importantly, IL-33 induced maturation and regulated the function of DCs by increasing expression of DCs mature markers (CD40 and CD80, CD86) DCs-function-related gene including antigen presentation genes (HLA-DMA, HLA-DMB and CD74) and cytokines (IL-1β, IL-6 and TNF). Mechanistic studies demonstrated that IL-33 treatment induced DCs maturation by upregulating CYLD expression in DCs. In addition, CYLD played an important role in DCs-induced T cell proliferation and IL-17 secretion. In conclusion, our study demonstrated that IL-33 mediated immunoregulation in pulmonary adenocarcinoma by improving DC-induced T cell proliferation by upregulating CYLD expression.

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