Abstract

The fetal scarless phenotype is characterized by an attenuated inflammatory response, an extracellular matrix (ECM) comprised of increased levels of hyaluronan (HA), and elevated levels of TGFB3 compared to TGFB1. We have reported a novel role for the anti-inflammatory cytokine, IL-10, in the fetal regenerative phenotype and its ability to induce scarless healing in adult wounds. Further, we have demonstrated a new non- immunologic mechanism for IL-10, which is regulation of HA. The TGF beta isoforms have also been implicated in HA regulation.

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