Evidence map›Paper›PMID 30290124›Full record

ArticleAmerican journal of respiratory cell and molecular biology2019

Myeloid TBK1 Signaling Contributes to the Immune Response to Influenza.

Robert S Hagan, Jose Torres-Castillo, Claire M Doerschuk

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Macrophage TBK1 signaling drives the development and outgrowth of breast cancer brain metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. The role of TBK1 in cancer pathogenesis and anticancer immunity.Journal of experimental & clinical cancer research : CR · 2022
    Review
  12. Article
  13. Review
  14. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Robert S Hagan1 Division of Pulmonary Diseases and Critical Care Medicine, Department of Medicine.ORCID 0000-0002-1504-0086
Jose Torres-Castillo1 Division of Pulmonary Diseases and Critical Care Medicine, Department of Medicine.
Claire M Doerschuk1 Division of Pulmonary Diseases and Critical Care Medicine, Department of Medicine.
Lung Institute · USUniversity of North Carolina at Chapel Hill · US

Funding

Rho-mediated Signaling in Lung Endothelial Cells Induced by Neutrophil AdhesionR01HL114388 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BURRIDGE, KEITH, DOERSCHUK, CLAIRE M · 2012 to 2016
$3.0M
Trafficking and function of macrophage subpopulations within the lung microenvironment during pneumoniaR01HL145396 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DOERSCHUK, CLAIRE M · 2019 to 2022
$2.3M
Application of Omics in Lung DiseaseK12HL119998 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DOERSCHUK, CLAIRE M · 2013 to 2017
$1.4M
Macrophage and monocyte TBK1 function in host defense against influenzaK08HL143271 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HAGAN, ROBERT STEWART · 2019 to 2021
$535k
NHLBI NIH HHS K08 HL143271NHLBI NIH HHS K12 HL119998NHLBI NIH HHS R01 HL114388NHLBI NIH HHS R01 HL145396
6 · The paper itself

Abstract

Macrophages provide key elements of the host response to influenza A virus (IAV) infection, including expression of type I IFN and inflammatory cytokines and chemokines. TBK1 (TNF receptor-associated factor family member-associated NF-κB activator-binding kinase 1) contributes to IFN expression and antiviral responses in some cell types, but its role in the innate response to IAV in vivo is unknown. We hypothesized that macrophage TBK1 contributes to both IFN and non-IFN components of host defense and IAV pathology. We generated myeloid-conditional TBK1 knockout mice and assessed the in vitro and in vivo consequences of IAV infection. Myeloid-specific loss of TBK1 in vivo resulted in less severe host response to IAV, as assessed by decreased mortality, weight loss, and hypoxia and less inflammatory changes in BAL fluid relative to wild-type mice despite no differences in viral load. Mice lacking myeloid TBK1 showed less recruitment of CD64

Indexed as

AnimalsCytokinesInfluenza A Virus, H1N1 SubtypeLungMacrophages, AlveolarMiceMice, Inbred C57BLMice, KnockoutMyeloid CellsNF-kappa BOrthomyxoviridae InfectionsPneumoniaProtein Serine-Threonine KinasesSignal TransductionCytokinesNF-kappa BProtein Serine-Threonine KinasesTbk1 protein, mousecytokineIFNinfluenzamacrophageTBK1

Identifiers

PMID30290124
PMCPMC6397979
OpenAlexW2894672650

What OpenQuestion holds

Textmetadata
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.