A role for T-bet-mediated tumour immune surveillance in anti-IL-17A treatment of lung cancer.

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info:eu-repo/semantics/altIdentifier/doi/10.1038/ncomms1609

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info:eu-repo/semantics/altIdentifier/pmid/22186896

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info:eu-repo/semantics/altIdentifier/eissn/2041-1723

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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_3676BCF1B3D99

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S. Reppert et al., « A role for T-bet-mediated tumour immune surveillance in anti-IL-17A treatment of lung cancer. », Serveur académique Lausannois, ID : 10.1038/ncomms1609


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Lung cancer is the leading cause of cancer deaths worldwide. The cytokine interleukin-17A supports tumour vascularization and growth, however, its role in lung cancer is unknown. Here we show, in the lungs of patients with lung adenocarcinoma, an increase in interleukin-17A that is inversely correlated with the expression of T-bet and correlated with the T regulatory cell transcription factor Foxp3. Local targeting of interleukin-17A in experimental lung adenocarcinoma results in a reduction in tumour load, local expansion of interferon-γ-producing CD4(+) T cells and a reduction in lung CD4(+)CD25(+)Foxp3(+) regulatory T cells. T-bet((-/-)) mice have a significantly higher tumour load compared with wild-type mice. This is associated with the local upregulation of interleukin-23 and induction of interleukin-17A/interleukin-17R-expressing T cells infiltrating the tumour. Local anti-interleukin-17A antibody treatment partially improves the survival of T-bet((-/-)) mice. These results suggest that local anti-interleukin-17A antibody therapy could be considered for the treatment of lung tumours.

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