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Tumor-associated macrophages (TAMs) are a major component of the tumor microenvironment and primarily exist as M2-like macrophages, which support tumor growth and suppress anti-tumor immunity. Repolarizing TAMs from the M2 to M1 phenotype is a promising therapeutic strategy. M1 macrophages secrete pro-inflammatory cytokines and promote anti-tumor immunity, while M2 macrophages secrete anti-inflammatory cytokines and support tumor progression. Repolarization strategies involve targeting signaling pathways, metabolic processes, epigenetic regulation, and using agonists for pattern recognition receptors to shift TAMs from an immunosuppressive/pro-tumoral state to an inflammatory/tumoricidal one. High infiltration of M2-polarized TAMs correlates with poor prognosis in many cancers, making repolarization a valuable therapeutic approach.
Repolarization of M2 macrophages to M1 macrophages within the tumor microenvironment, leading to enhanced anti-tumor immunity and reduced tumor progression. This involves shifting the cytokine profile, modulating signaling pathways (STAT, NF-kB), and altering metabolic processes within the macrophages.
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