Immunology Microbiology Lab, Department of Human Physiology, Tripura University, Suryamaninagar, Tripura 799022, India.
Immunology Microbiology Lab, Department of Human Physiology, Tripura University, Suryamaninagar, Tripura 799022, India; Department of Integrative Immunobiology, Duke University Medical Center, Durham, NC 27710, USA.
Life Sci. 2024 Sep 1;352:122896. doi: 10.1016/j.lfs.2024.122896. Epub 2024 Jul 6.
Despite significant advancements in cancer treatment in recent decades, the high mortality rate associated with lung cancer remains a significant concern. The development and proper execution of new targeted therapies needs more deep knowledge regarding the lung cancer associated tumour microenvironment. One of the key component of that tumour microenvironment is the lung resident macrophages. Although in normal physiological condition the lung resident macrophages are believed to maintain lung homeostasis, but they may also initiate a vicious inflammatory response in abnormal conditions which is linked to lung cancer development. Depending on the activation pathway, the lung resident macrophages are either of M1 or M2 sub-type. The M1 and M2 sub-types differ significantly in various prospectuses, from phenotypic markers to metabolic pathways. In addition to this generalized classification, the recent advancement of the multiomics technology is able to identify some other sub-types of lung resident macrophages. Researchers have also observed that these different sub-types can manipulate the pathogenesis of lung carcinogenesis in a context dependent manner and can either promote or inhibit the development of lung carcinogenesis upon receiving proper activation. As proper knowledge about the role played by the lung resident macrophages' in shaping the lung carcinogenesis is limited, so the main purpose of this review is to bring all the available information under the same roof. We also elaborated the different mechanisms involved in maintenance of the plasticity of M1/M2 sub-type, as this plasticity can be a good target for lung cancer treatment.
尽管近几十年来癌症治疗取得了重大进展，但与肺癌相关的高死亡率仍然是一个重大问题。新的靶向治疗的开发和正确实施需要更深入地了解与肺癌相关的肿瘤微环境。该肿瘤微环境的一个关键组成部分是肺驻留巨噬细胞。虽然在正常生理条件下，肺驻留巨噬细胞被认为维持着肺的内稳态，但在异常条件下，它们也可能引发恶性炎症反应，从而导致肺癌的发展。根据激活途径的不同，肺驻留巨噬细胞分为 M1 或 M2 亚型。M1 和 M2 亚型在表型标志物到代谢途径等各个方面都有显著差异。除了这种广义分类外，多组学技术的最新进展能够识别其他一些肺驻留巨噬细胞亚型。研究人员还观察到，这些不同的亚型可以根据具体情况来操纵肺癌发生的发病机制，并在接收到适当的激活后促进或抑制肺癌的发生。由于对肺驻留巨噬细胞在塑造肺癌发生中的作用的了解有限，因此本综述的主要目的是将所有可用信息汇集在一起。我们还详细阐述了维持 M1/M2 亚型可塑性的不同机制，因为这种可塑性可能是治疗肺癌的一个很好的靶点。
