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At later stages, lipid mediators such as resolvins, anti-inflammatory cytokines and cellular processes such as efferocytosis (the phagocytosis of apoptotic cells) downregulate the M1-like phenotype and induce an M2-like phenotype [40-44].
[104] designed iron oxide-loaded liposomes decorated with phosphatidylserine (PS), a cell surface ligand displayed on apoptotic cells that triggers macrophage uptake and a subsequent phenotypic switch to an M2-like phenotype, enabling macrophage phenotype ma- nipulation as well as imaging and tracking by magnetic resonance
Near the end of wound healing, during resolution, dermal macrophages self-renew, and clear apoptotic cells as the tissue returns to homeostasis (Davies et al.
Although early research investigating the contribution of mac- rophages to wound repair focused on their role as scavenger cells that phagocytize cellular debris, invading organisms, neu- trophils, and other apoptotic cells after tissue injury (Peiser et al.
Finally, by mimicking the anti-inflam- matory effects of apoptotic cells, phosphatidlyserine-presenting liposomes have also been used to induce reparative IL-10- and TGFb1-producing cardiac macrophages (Harel-Adar et al.
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