Research ArticleCancer Immunology

IL-33 and ST2 mediate FAK-dependent antitumor immune evasion through transcriptional networks

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Science Signaling  05 Dec 2017:
Vol. 10, Issue 508, eaan8355
DOI: 10.1126/scisignal.aan8355

FAK directs tumor immune evasion

Tumors are adept at escaping the immune system’s surveillance or suppressing its activity. The kinase FAK is implicated in immune escape mechanisms. Serrels et al. found that FAK activates a transcriptional network that induces—and is then further mediated by—the nuclear abundance of interleukin-33 (IL-33) in tumor cells. In a mouse model of squamous cell carcinoma, FAK–IL-33 complexes boosted the production and secretion of two key factors in immunosuppression: the chemokine CCL5, which stimulates immunosuppressive regulatory T cells, and soluble ST2, a decoy receptor for cytotoxic T cell–stimulatory IL-33. Blocking these FAK-mediated signals may help the patient’s immune system find and kill tumors.

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