GM-CSF regulates alveolar macrophage differentiation and innate immunity in the lung through PU.1.
By Y. Shibata, P. Berclaz, Z. Chroneos, Mitsuhiro Yoshida, Jeffrey A. Whitsett, B. Trapnell. Immunity, 2001
622 citations recorded by the source corpus.
GM-CSF gene targeted (GM(-/-)) mice are susceptible to respiratory infections and develop alveolar proteinosis due to defects in innate immune function and surfactant catabolism in alveolar macrophages (AMs), respectively. Reduced cell adhesion, phagocytosis, pathogen killing, mannose- and Toll-like receptor expression, and LPS- or peptidoglycan-stimulated TNFalpha release were observed in AMs from GM(-/-) mice. The transcription factor PU.1 was markedly reduced in AMs of GM(-/-) mice in vivo and was restored by selective expression of GM-CSF in the lungs of SPC-GM/GM(-/-) transgenic mice. Retrovirus-mediated expression of PU.1 in AMs from GM(-/-) mice rescued host defense functions and surfactant catabolism by AMs. We conclude that PU.1 mediates GM-CSF-dependent effects on terminal differentiation of AMs regulating innate immune functions and surfactant catabolism by AMs.
Subfields: Immunology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/634c9adb019a47e78260f0646b3cb7293570f419
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In Immunology
Citations in the corpus
- Pulmonary alveolar proteinosis: progress in the first 44 years. (2002, methodology): “Numerous defects in phagocytosis have been described, including reduced uptake of fluorescein isothiocyanate (FITC)-labeled microspheres [62,63, 104,105], whether exposed in vitro or in vivo, transferrin-labeled microspheres [104] and large diameter latex spheres [104].”
- Alveolar macrophages develop from fetal monocytes that differentiate into long-lived cells in the first week of life via GM-CSF (2013, neutral): “, 2007), or that AMF development was abnormal (Shibata et al., 2001).”
- From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation (2014, background): “CSF-1 is also involved in the proliferation of splenic red pulp macrophages and bone marrow macrophages (110).”