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tgfb_im

Bioinformatics analyses in the report by Peng et al.

https://github.com/blanqwall/tgfb_im

Science Score: 67.0%

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    CITATION.cff file
    Found CITATION.cff file
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    codemeta.json file
    Found codemeta.json file
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    .zenodo.json file
    Found .zenodo.json file
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    DOI references
    Found 2 DOI reference(s) in README
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    Academic publication links
    Links to: zenodo.org
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    Low similarity (4.0%) to scientific vocabulary
Last synced: 9 months ago · JSON representation ·

Repository

Bioinformatics analyses in the report by Peng et al.

Basic Info
  • Host: GitHub
  • Owner: BlanQwall
  • Language: R
  • Default Branch: main
  • Size: 29.9 MB
Statistics
  • Stars: 0
  • Watchers: 1
  • Forks: 0
  • Open Issues: 0
  • Releases: 2
Created over 1 year ago · Last pushed over 1 year ago
Metadata Files
Readme Citation

README.md

A lung Tgf-beta-signaling-mediated endothelial-interstitial macrophage axis prevents age-related abnormalities

This repertoire represents the bioinformatics analyses in the report by Peng et al.

Code source is also available on Zenodo: DOI

Abstract:

Lung interstitial macrophages (IMs) are monocyte-derived parenchymal macrophages whose homeostatic and tissue-supportive functions remain unclear. While recent progress has been made about the diversity and transcriptional regulation of lung IMs, the microenvironmental signals responsible for their development from monocytes and for their functional specification remain unidentified. Here we found, in mice, that lung endothelial cell-derived Tgf-beta1 specifically triggered a core Tgf-beta receptor-dependent IM signature in bone marrow-derived monocytes and macrophages (Macs). In vivo, myeloid-specific ablation of Tgf-beta receptor signaling severely impaired monocyte-to-IM development, resulting in the accumulation of perivascular monocytes, decreased IM numbers and a loss of IM-intrinsic identity. Of note, monocyte-to-IM development was similarly impaired in the absence of endothelial-specific Tgf-beta1. Functionally, lungs from mice selectively lacking Tgf-beta receptor in IMs exhibited spatial changes in monocyte and IM niche occupancies, a severe disruption in their immunoregulatory environment, and prematurely developed fibrosis, hyperinflation, increased compliance and decreased elastance, changes classically associated with aging. Our work identifies a novel endothelial – IM axis involving Tgf-beta1- Tgf-beta receptor interactions that shapes IM development and identity and thereby sustains lung tissue integrity, thus providing foundations for IM-targeted interventions in the context of lung aging and other chronic inflammatory disorders.

Owner

  • Name: BAI Qiang
  • Login: BlanQwall
  • Kind: user
  • Location: Montpellier, France
  • Company: PhyMedExp | INSERM U1046

Citation (CITATION.cff) 

cff-version: 1.1.0
message: "The codes used for bioinformatics analysis in Peng et al. 2025. Science Immunology."
authors:
- family-names: Bai
  given-names: Qiang
orcid: https://orcid.org/0000-0001-7423-0712
title:BlanQwall/TGFb_IM: New release for archiving in Zenodo
version: v1.0.0
date-released: 2025-03-05

GitHub Events

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  • Release event: 2
  • Push event: 3
  • Public event: 1
  • Create event: 2
Last Year
  • Release event: 2
  • Push event: 3
  • Public event: 1
  • Create event: 2