Evidence map›Paper›PMID 27881705›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

Essential Role of mTORC1 in Self-Renewal of Murine Alveolar Macrophages.

Wenhai Deng, Jialong Yang, Xingguang Lin, Jinwook Shin, Jimin Gao, Xiao-Ping Zhong

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025
    Review
  5. RACK1 promotes the development and function of alveolar macrophages through directly binding to and stabilizing PPARγ.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Article
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  11. Review
  12. Article
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  14. Article
  15. Rate of recipient-derived alveolar macrophage development and major histocompatibility complex cross-decoration after lung transplantation in humans.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
    Article
  16. Article
  17. Review
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  19. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Wenhai DengSchool of Laboratory Medicine, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
Jialong YangDivision of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC 27710.
Xingguang LinSchool of Laboratory Medicine, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
Jinwook ShinDivision of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC 27710.ORCID 0000-0003-3476-7595
Jimin GaoSchool of Laboratory Medicine, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China; xiaoping.zhong@duke.edu jimingao@yahoo.com.ORCID 0000-0002-3911-043X
Xiao-Ping ZhongDivision of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC 27710; xiaoping.zhong@duke.edu jimingao@yahoo.com.ORCID 0000-0002-4619-8783
Duke Medical Center · USWenzhou Medical University · CN

Funding

Regulation of peripheral T cell toleranceR01AI079088 · NIAID · DUKE UNIVERSITY · PI ZHONG, XIAOPING · 2008 to 2019
$3.5M
TSC1-mTOR signaling and T cell toleranceR01AI101206 · NIAID · DUKE UNIVERSITY · PI ZHONG, XIAOPING · 2012 to 2016
$1.9M
NIAID NIH HHS R01 AI079088NIAID NIH HHS R01 AI101206
6 · The paper itself

Abstract

Alveolar macrophages (AMϕ) have the capacity of local self-renewal through adult life; however, mechanisms that regulate AMϕ self-renewal remain poorly understood. We found that myeloid-specific deletion of Raptor, an essential component of the mammalian/mechanistic target of rapamycin complex (mTORC)1, resulted in a marked decrease of this population of cells accompanying altered phenotypic features and impaired phagocytosis activity. We demonstrated further that Raptor/mTORC1 deficiency did not affect AMϕ development, but compromised its proliferative activity at cell cycle entry in the steady-state as well as in the context of repopulation in irradiation chimeras. Mechanically, mTORC1 confers AMϕ optimal responsiveness to GM-CSF-induced proliferation. Thus, our results demonstrate an essential role of mTORC1 for AMϕ homeostasis by regulating proliferative renewal.

Indexed as

AnimalsCell ProliferationFlow CytometryHomeostasisMacrophages, AlveolarMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMice, KnockoutMultiprotein ComplexesReal-Time Polymerase Chain ReactionTOR Serine-Threonine KinasesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesTOR Serine-Threonine Kinases

Identifiers

PMID27881705
PMCPMC5173435
OpenAlexW2549632928

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.