Department of Microbiology, Asutosh College, 92, S. P. Mukherjee Road, Kolkata 700026, India.
Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata 700026, India.
Clin Immunol. 2021 Nov;232:108875. doi: 10.1016/j.clim.2021.108875. Epub 2021 Nov 2.
Inflammation is a part of carefully co-ordinated healing immune exercise to eliminate injurious stimuli. However, in substantial number of cancer types, it contributes in shaping up of robust tumor microenvironment (TME). Solid TME promotes infiltration of tumor associated macrophages (TAMs) that contributes to cancer promotion. TAMs are functionally heterogeneous and display an extraordinary degree of plasticity, which allow 'Switching' of macrophages into an 'M2', phenotype, linked with immunosuppression, advancement of tumor angiogenesis with metastatic consequences. In contrary to the classical M1 macrophages, these M2 TAMs are high-IL-10, TGF-β secreting-'anti-inflammatory'. In this review, we will discuss the modes of infiltration and switching of TAMs into M2 anti-inflammatory state in the TME to promote immunosuppression and inflammation-driven cancer.
炎症是一种精心协调的免疫修复活动，旨在消除有害刺激。然而，在大量癌症类型中，炎症有助于形成强健的肿瘤微环境（TME）。坚实的 TME 促进了肿瘤相关巨噬细胞（TAMs）的浸润，而这些巨噬细胞则促进了癌症的发生。TAMs 在功能上具有异质性，并表现出非凡的可塑性，这使得巨噬细胞能够“切换”为与免疫抑制、肿瘤血管生成以及转移后果相关的“M2”表型。与经典的 M1 巨噬细胞不同，这些 M2 TAMs 高分泌 IL-10 和 TGF-β，是“抗炎”的。在这篇综述中，我们将讨论 TAMs 浸润和向 M2 抗炎状态转换的方式，以促进免疫抑制和炎症驱动的癌症。
