烟草及PM2.5影响肺癌免疫治疗的研究进展

Impact of tobacco and PM2.5 on lung cancer immunotherapy

摘要:

肺癌作为全球癌症相关死亡的首要原因，其发生与多种环境因素密切相关。吸烟、空气污染等环境危险因素会对肺部细胞造成不同程度的损伤，并引发炎症反应。在这一过程中，机体的免疫系统会被激活，试图清除受损细胞和潜在的癌变细胞。然而，环境因素的持续作用可能会导致免疫应答异常。一方面，烟草中的有害物质可直接损伤免疫细胞，抑制免疫细胞的增殖与功能，从而削弱免疫系统对肺癌细胞的识别和清除能力。另一方面，空气污染中的细颗粒物 （PM_2.5 ） 可进入肺组织，激活炎症信号通路，促使炎症因子大量释放，诱导免疫抑制微环境的形成，使肺癌细胞得以逃避免疫监视。 这些环境因素通过影响肺癌的免疫应答，在肺癌的发生发展中扮演着重要角色。本文综述烟草及PM_2.5与肺癌及免疫治疗的关系，旨在为肺癌的预防和治疗提供新的思路。

Abstract:

Lung cancer remains the leading cause of cancer-related mortality worldwide, with its etiology closely associated with multiple environmental risk factors. Environmental risk factors, such as smoking and air pollution, induce varying degrees of damage to pulmonary cells and trigger inflammatory responses. During this process, the body's immune system is activated to eliminate damaged cells and potential malignant cells. However, prolonged exposure to these environmental factors may disrupt normal immune function. On the one hand, harmful components in tobacco directly damage immune cell viability and functionality, thus diminishing the immune system's ability to recognize and eliminate lung cancer cells. On the other hand, fine particulate matter (PM2.5) in polluted air penetrates pulmonary tissues, activates inflammatory signaling pathways, promotes excessive release of pro-inflammatory cytokines, fostering an immunosuppressive microenvironment that enables cancer cells to evade immune surveillance. These environmental factors play a critical role in lung cancer initiation and progression by modulating immune responses. This review focuses on the interplay between tobacco / PM2.5 exposure, lung cancer, and immunotherapy, aiming to propose novel strategies for lung cancer prevention and therapeutic innovation.