TGF-β Gives an Air of Exclusivity to Alveolar Macrophages Bart N. Lambrecht  Immunity  Volume 47, Issue 5, Pages 807-809 (November 2017) DOI: 10.1016/j.immuni.2017.11.005 Copyright © 2017 Elsevier Inc. Terms and Conditions

Figure 1 Development of AMs Is Regulated by Autocrine TGF-β Around embryonic day E18.5, fetal monocytes accumulate in the lungs and differentiate into pre-alveolar macrophages (pre-AM) under the influence of granulocyte-macrophage colony-stimulating factor (GM-CSF). They also start producing transforming growth factor-β (TGF-β) that acts in concert with GM-CSF. Around the day of birth (DOB), the pre-AMs cross the alveolo-capillary membrane involved in gas exchange to reside in the air-exposed parts of the lung and occupy their niche as tissue resident macrophages. Here, AMs encounter surfactant, which they start ingesting and metabolizing. Again, TGF-β and GM-CSF are crucial for inducing the transcription factor PPARγ that controls surfactant metabolism and induces further maturation of pre-AMs into fully mature AMs that firmly adhere to the alveolar epithelial cells (AEC), and perform key functions in lung homeostasis. This maturation process is accompanied by upregulation of key surface molecules like CD64, SiglecF, CD11c, and with downregulation of CD11b. Immunity 2017 47, 807-809DOI: (10.1016/j.immuni.2017.11.005) Copyright © 2017 Elsevier Inc. Terms and Conditions