Zhu Lin, Jin Zhi
Department of Traditional Chinese Medicine, The Second Hospital of Shandong University, Jinan, China.
Front Oncol. 2024 Aug 29;14:1345765. doi: 10.3389/fonc.2024.1345765. eCollection 2024.
Lung cancer is a major health burden globally and smoking is a well-known risk factor. It has been observed that chronic inflammation contributes to lung cancer progression, with immune cells and inflammatory cytokines implicated in tumor development. Clarifying the causal links between these immune components and lung cancer could enhance prevention and therapy.
We performed Mendelian randomization (MR) to explore causal connections between immune cells, inflammatory markers, and lung cancer risk, using genetic variants as instruments. Data from GWAS on these variables underpinned our MR analyses.
Our findings indicated an inverse association between some immune cells and lung cancer risk, implying that more immune cells might be protective. NK T cells (CD16-CD56) and myeloid cells (HLA DR+ on CD33dim HLA DR+ CD11b+) had an inverse correlation with lung cancer risk. Furthermore, a direct relationship was observed between inflammatory cytokines and these immune cells. In contrast, IL-18 was inversely associated with lung cancer, while IL-13 showed a direct correlation.
The study underscores the role of immune and inflammatory factors in lung cancer. These insights could lead to new therapeutic strategies for combating lung cancer.
肺癌是全球主要的健康负担，吸烟是众所周知的风险因素。据观察，慢性炎症会促进肺癌进展，免疫细胞和炎性细胞因子与肿瘤发展有关。阐明这些免疫成分与肺癌之间的因果关系有助于预防和治疗。
我们进行了孟德尔随机化（MR）研究，以探索免疫细胞、炎症标志物与肺癌风险之间的因果联系，使用基因变异作为工具。关于这些变量的全基因组关联研究（GWAS）数据支持了我们的MR分析。
我们的研究结果表明，一些免疫细胞与肺癌风险呈负相关，这意味着更多的免疫细胞可能具有保护作用。自然杀伤T细胞（CD16-CD56）和髓样细胞（CD33dim HLA DR+ CD11b+上的HLA DR+）与肺癌风险呈负相关。此外，观察到炎性细胞因子与这些免疫细胞之间存在直接关系。相比之下，白细胞介素-18与肺癌呈负相关，而白细胞介素-13呈正相关。
该研究强调了免疫和炎症因素在肺癌中的作用。这些见解可能会带来对抗肺癌的新治疗策略。
