TGF-β1 increases expression of the regulatory receptor CD200R on AMs, ligation of which by CD200 on epithelial cells limits their pro-inflammatory response to influenza infection.45 Mice lacking αVβ6 integrin on airway epithelial cells display spontaneous AM activation46 and develop emphysema due to overproduction of the AM-derived matrix metalloproteinase (MMP) 12,38 suggesting that local TGF-β activity maintains their homeostatic phenotype. The gene discussed is TGFB1; the disease is pulmonary emphysema.