A role for T-bet-mediated tumour immune surveillance in anti-IL-17A treatment of lung cancer
Menée sur un modèle murin, cette étude suggère qu'un traitement local par anticorps anti-interleukine-17A réduit la croissance d'une tumeur pulmonaire
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.