Evidence map›Paper›PMID 34547174›Full record

ArticleAging cell2021

Type I Interferon signaling controls the accumulation and transcriptomes of monocytes in the aged lung.

Shanti S D'Souza, Yuanyue Zhang, Jacob T Bailey, Ivan T H Fung, Marcy L Kuentzel, Sridar V Chittur, Qi Yang

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
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  7. Article
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  10. Aging and Inflammation.Cold Spring Harbor perspectives in medicine · 2024
    Review
  11. Article
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  13. Review
  14. Review
  15. Article
  16. The Roles of Myeloid Cells in Aging-related Liver Diseases.International journal of biological sciences · 2023
    Review
  17. Article
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  19. Article
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

7 authors at 2 institutions in 1 country.

Shanti S D'SouzaDepartment of Immunology and Microbial Disease, Albany Medical College, Albany, NY, USA.
Yuanyue ZhangDepartment of Immunology and Microbial Disease, Albany Medical College, Albany, NY, USA.
Jacob T BaileyDepartment of Immunology and Microbial Disease, Albany Medical College, Albany, NY, USA.
Ivan T H FungDepartment of Immunology and Microbial Disease, Albany Medical College, Albany, NY, USA.
Marcy L KuentzelCenter for Functional Genomics, University at Albany-SUNY, Rensselaer, NY, USA.
Sridar V ChitturCenter for Functional Genomics, University at Albany-SUNY, Rensselaer, NY, USA.
Qi YangDepartment of Immunology and Microbial Disease, Albany Medical College, Albany, NY, USA.ORCID 0000-0002-8365-0986
Albany Medical Center Hospital · USUniversity at Albany, State University of New York · US

Funding

Function and regulation of mucosal associated invariant T cells in the lungR01HL155021 · NHLBI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI YANG, QI · 2021 to 2025
$2.8M
Innate Lymphoid Cell AgingR01AG057782 · NIA · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI YANG, QI · 2017 to 2021
$1.7M
Development and function of inflammatory innate lymphoid cellsR01HL137813 · NHLBI · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI YANG, QI · 2018 to 2021
$1.6M
NHLBI NIH HHS R01 HL137813NHLBI NIH HHS R01 HL155021NIA NIH HHS R01 AG057782
6 · The paper itself

Abstract

Aging is paradoxically associated with a deteriorated immune defense (immunosenescence) and increased basal levels of tissue inflammation (inflammaging). The lung is particularly sensitive to the effects of aging. The immune cell mechanisms underlying physiological lung aging remain poorly understood. Here we reveal that aging leads to increased interferon signaling and elevated concentrations of chemokines in the lung, which is associated with infiltration of monocytes into the lung parenchyma. scRNA-seq identified a novel Type-1 interferon signaling dependent monocyte subset (MO-ifn) that upregulated IFNAR1 expression and exhibited greater transcriptomal changes with aging than the other monocytes. Blockade of type-1 interferon signaling by treatment with anti-IFNAR1 neutralizing antibodies rapidly ablated MO-ifn cells. Treatment with anti-IFNAR1 antibodies also reduced airway chemokine concentrations and repressed the accumulation of the overall monocyte population in the parenchyma of the aged lung. Together, our work suggests that physiological aging is associated with increased basal level of airway monocyte infiltration and inflammation in part due to elevated type-1 interferon signaling.

Indexed as

AgingAnimalsHumansInterferon Type ILungMiceMonocytesSignal TransductionTranscriptomeInterferon Type Iaginginterferon-stimulated geneslungmonocytestype 1 interferon

Identifiers

PMID34547174
PMCPMC8520712
OpenAlexW3200552777

What OpenQuestion holds

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LicenceCC BY
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.