HBEGF and pulmonary fibrosis: By using the CD11b-diphtheria toxin receptor (DTR) in transgenic mice to establish an IL-13-dependent model, Borthwick et al. [19] demonstrated that lung fibrosis and inflammation crucially rely on monocyte-derived AMs to maintain type-2 immunity, and AMs may harness this role by regulating chemokine production and recruiting effector T cells to the lungs.