This study identifies a new role for the transcription regulator BACH2 in alveolar macrophage (AM) function and lung homeostasis. Bach2−/− mice were shown to develop pulmonary alveolar proteinosis-like disease, which comprised an accumulation of surfactants and infiltration of granulocytes and AMs in the lungs. Compared with wild-type AMs, Bach2−/− AMs showed increased uptake of surfactant lipids and impaired cholesterol metabolism, which contributed to a foamy appearance. Moreover, they had an altered expression of genes involved in chemotaxis (which probably contributed to the granulocyte infiltration) and showed a bias towards alternative M2 macrophage activation, which suggests that BACH2 normally limits M2 polarization. Importantly, the disease could be relieved by wild-type bone marrow transfer, which supports the key role for AMs in lung homeostasis.
References
Nakamura, A. et al. Transcription repressor Bach2 is required for pulmonary surfactant homeostasis and alveolar macrophage function. J. Exp. Med. 210, 2191–2204 (2013)
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Bird, L. BACH2 normal. Nat Rev Immunol 13, 849 (2013). https://doi.org/10.1038/nri3580
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DOI: https://doi.org/10.1038/nri3580