近日,，國際著名雜志Nature Communications刊登了德國埃朗根－紐倫堡大學醫(yī)院研究人員的最新研究成果“A role for T-bet-mediated tumour immune surveillance in anti-IL-17A treatment of lung cancer”，文章中指出,，該院研究人員開發(fā)出一種治療肺癌的新方法,，通過引入抗體阻斷一種促進腫瘤生長的“信使物質”,，可提高肺癌患者的存活率。
據介紹,，研究人員發(fā)現人體免疫系統(tǒng)中一種名為白介素－17A的“信使物質”會促進腫瘤生長,，而這種物質往往會在肺癌患者體內大量出現。
摸清了免疫系統(tǒng)的“工作流程”后,，研究人員開始探索治療肺癌的新方法,，結果發(fā)現，引入某種抗體“封鎖”上述“信使物質”后,，可有效抑制腫瘤增長,，提高患者存活率。此外,，研究人員沒有采取傳統(tǒng)的注射方法給患者引入抗體,，而是通過滴鼻劑的方式引入。
據世界衛(wèi)生組織的數據，肺癌不但是最常見的一種癌癥,，它導致的死亡人數也比其它癌癥高。（生物谷Bioon.com）
doi:10.1038/ncomms1609
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A role for T-bet-mediated tumour immune surveillance in anti-IL-17A treatment of lung cancer
S. Reppert,I. Boross,M. Koslowski,Ö. Türeci,S. Koch,H.A. Lehr&S. Finotto
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.
