9/7/2023 0 Comments Jing gao google scholar ncarM1 macrophages, which are stimulated by interferon (IFN)-γ (produced by T-helper 1 cells) and bacterial lipopolysaccharide, are generally considered to have pro-inflammatory and anti-tumor effects and express inflammatory factors including interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. Due to the plasticity of macrophages, undifferentiated macrophages (M0) can be polarized into two types: classically activated macrophages (M1) and alternatively activated macrophages (M2) ( 2). Macrophages are involved in host defense, wound healing, and immune regulation and differentiate into different phenotypes in response to environmental cues ( 1). Hence, understanding the role of signaling pathways associated with TAM polarization and approaches that can regulate TAM repolarization provide a new perspective for cancer therapy. Modulation of TAMs by regulating M1 signaling activation has emerged as a promising and novel immunotherapy strategy. Current cancer treatment strategies are not limited to traditional radiotherapy, chemotherapy, or surgical resection as cancer treatment has entered the era of targeted therapy and immunotherapy. TAMs are generally M2-like anti-inflammatory immune cells and are associated with malignant disease progression, drug resistance, and poor prognosis. Therefore, macrophages that infiltrate the tumor microenvironment (TME), also known as tumor-associated macrophages (TAMs), have gradually attracted attention. Under the stimulation of various cytokines, macrophages can be polarized into two forms that exhibit different functions: M1 macrophages, which are pro-inflammatory and tumor-inhibiting, and M2 macrophages, which are anti-inflammatory and tumor-supporting. Furthermore, there is a close relationship between macrophages and tumors. Macrophages are an important part of the mononuclear phagocytic system and are involved in immune system regulation, pathogen clearance, wound healing, and angiogenesis.
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