TGFB1 and Intraalveolar phospholipid accumulation: For instance, given AMs are in direct contact with surfactant (produced by alveolar type 2 epithelial cells) and invading pathogens, a defect in GM-CSF or TGFβ signalling leads to accumulation of surfactant (alveolar proteinosis) and increased susceptibility to pulmonary infections (Baker et al., 2010; Huffman et al., 1996).