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(PPAR?) activation during CGD inflammation is deficient, leading to altered macrophage programming and decreased efferocytosis, and that PPAR? agonism would enhance resolution. using the gp91(phox-/-) murine model of X-linked CGD in a well-characterized model of sterile, zymosan-induced peritonitis, it was demonstrated that PPAR? expression and activation in CGD macrophages were significantly deficient at baseline, and acquisition was delayed over the course of inflammation relative to that of wild-type.]. 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