CSF2 and infection: The present study is not confounded by prior immaturity of AMs and defective surfactant catabolism, nor potential defects in migratory dendritic cell subsets, NK cells, and other myeloid cells outside the alveolar compartment in the lung and in other tissues of Csf2−/− mice [62–65], or disruption of GM-CSF secretion by immune and non-immune cells that may elaborate GM-CSF in response to infection.