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M2 macrophage markers refer to a diverse set of proteins and signaling molecules used to identify alternatively activated (M2) macrophages, which are primarily involved in anti-inflammatory responses, tissue repair, and the resolution of inflammation (Roszer, 2015). Key markers include surface receptors such as CD163 and CD206 (Mannose Receptor), as well as the intracellular enzyme Arginase-1 (ARG1), which plays a pivotal role in metabolic shifts that suppress T-cell activity (Munder, 2009). In the context of oncology, M2-polarized tumor-associated macrophages (TAMs) are frequently identified by these markers and are known to facilitate tumor growth, angiogenesis, and immune evasion (Yunna et al., 2020). While these markers are not typically therapeutic targets themselves, they are essential for characterizing the immune landscape of the tumor microenvironment and for monitoring the efficacy of drugs designed to deplete or reprogram M2-like cells into pro-inflammatory M1-like cells (Cassetta & Pollard, 2018). Therapeutic strategies targeting the M2 phenotype include CSF1R inhibitors like pexidartinib and inhibitors of M2-polarizing cytokines such as IL-4 and IL-13.
Reprogramming of macrophage polarization from M2 to M1, depletion of M2-like tumor-associated macrophages, or inhibition of M2-inducing cytokines.
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