Survival and Homeostasis of Alveolar Macrophages in Vivo Depend on mTOR Signaling

Hennessy-Strahs S, Su X, Sun S, Deng G, Muo W, Li Jiarui, Miller T, Xiao X, Li XC · 2026 · American Journal of Respiratory Cell and Molecular Biology · Atlas ID HEN2026

What this study shows

Myeloid-specific deletion of mTOR (and pharmacologic mTOR inhibition with temsirolimus) causes progressive depletion of alveolar macrophages, impaired phagocytosis, lipid accumulation and PAP-like lung pathology in mice, identifying mTOR as a nonredundant regulator of alveolar macrophage survival — mechanistic support for mTOR-inhibitor-associated pulmonary toxicity.

Abstract

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Alveolar homeostasis depends on tissue-resident professional phagocytes known as alveolar macrophages (AMs) that catabolize pulmonary surfactant. Pulmonary alveolar proteinosis (PAP) arises from impaired surfactant clearance due to loss or dysfunction of AMs, most commonly from disrupted GM-CSF-dependent AM homeostasis and less frequently from congenital defects in surfactant synthesis or processing. PAP has also been reported as a pulmonary toxicity associated with mTOR inhibitor-based immunosuppressive therapy.

Read the full abstract on PubMed →

At a glance

Evidence type	A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse (myeloid-specific Mtor deletion); GM-CSF-driven alveolar-macrophage-like cell culture (in vitro)); the code names the system studied -- animal work can be rigorous and still not be human data.
Study type	4 - Animal Study
Model system	Mouse (myeloid-specific Mtor deletion); GM-CSF-driven alveolar-macrophage-like cell culture (in vitro)
Journal	American Journal of Respiratory Cell and Molecular Biology
Year	2026
Peer reviewed	Yes
Record last updated	2026-10-01
Source	DOI 10.1093/ajrcmb/aanag139 · PMID 42578718

Extracted findings

These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.

Intervention	Myeloid-specific Mtor genetic deletion; temsirolimus (pharmacologic mTOR inhibitor)
Target	mTOR / PPARgamma / Bcl-2 family
Model	Mouse (in vivo); GM-CSF-driven AM-like cells (in vitro)
Effect	mTOR loss (genetic or pharmacologic) depletes alveolar macrophages and causes PAP-like lung pathology; mTOR required for AM survival, phagocytosis and lipid handling

In the Atlas

Cite this paper

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Hennessy-Strahs, S., Su, X., Sun, S., Deng, G., Muo, W., Li Jiarui, Miller, T., Xiao, X., & Li, X. C. (2026). Survival and Homeostasis of Alveolar Macrophages in Vivo Depend on mTOR Signaling. American Journal of Respiratory Cell and Molecular Biology. https://doi.org/10.1093/ajrcmb/aanag139

@article{HEN2026,
  author       = {Hennessy-Strahs, S. and Su, X. and Sun, S. and Deng, G. and Muo, W. and Li Jiarui and Miller, T. and Xiao, X. and Li, X. C.},
  title        = {{Survival and Homeostasis of Alveolar Macrophages in Vivo Depend on mTOR Signaling}},
  journal      = {American Journal of Respiratory Cell and Molecular Biology},
  year         = {2026},
  doi          = {10.1093/ajrcmb/aanag139},
  note         = {PMID: 42578718},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper.

Barton, O. (2026). Oliver's mTOR Atlas (record HEN2026) [Data set]. https://mtor-atlas.org/study/HEN2026/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_HEN2026,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record HEN2026},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/HEN2026/},
  doi          = {10.5281/zenodo.22059963}
}

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