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Abstract Stem cell–based therapies offer potential for repairing large skeletal defects, yet persistent inflammation limits their efficacy. Here, we identify macrophage–derived IL-18 as an immune switch that impairs skeletal regeneration by disrupting immune–mesenchymal cell interactions. IL-18 is elevated in male mouse non-healing models and human bone nonunion samples, supporting its translational relevance.
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
