In the normal lung (A), only alveolar macrophages are present within the distal air spaces. After LPS-induced ALI (B), neutrophils and macrophages accumulate in the alveolar space and release inflammatory mediators that cause barrier dysfunction and pulmonary edema. In their study in mice in this issue of the JCI, D’Alessio et al. (13) report that effective resolution of this process involves CD4⁺CD25⁺ Tregs (C), which cause neutrophil apoptosis and efferocytosis and produce the proresolution mediator TGF-β upon contact with alveolar macrophages.