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Macrophage polarization to the M2 phenotype via IL-10 secretion is a crucial process in immune regulation, characterized by the adoption of an anti-inflammatory and tissue-repairing state. IL-10, acting as both an autocrine and paracrine factor, drives this polarization by suppressing pro-inflammatory cytokine secretion, enhancing anti-inflammatory gene expression, and promoting tissue remodeling. M2 macrophages polarized via IL-10 exhibit enhanced tissue remodeling/fibrosis potential, increased collagen deposition, and suppressed inflammatory responses, making them vital for wound healing but also implicated in pathological fibrosis and tumor progression. The balance between M1 and M2 phenotypes is critical in various diseases, and therapeutic modulation targeting this axis is under investigation.
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