Evidence map›Paper›PMID 23981064›Full record

ArticleImmunology2014

Mycobacterium tuberculosis infection of human dendritic cells decreases integrin expression, adhesion and migration to chemokines.

Lawton L Roberts, Cory M Robinson

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. HowVaccines · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Early innate cell interactions withFrontiers in immunology · 2023
    Review
  8. Glucose metabolism and its role in the maturation and migration of human CD1cFrontiers in cellular and infection microbiology · 2023
    Article
  9. Biomedicines · 2022
    Article
  10. Pathological and protective roles of dendritic cells inFrontiers in cellular and infection microbiology · 2022
    Review
  11. Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Microorganisms · 2020
    Article
  16. Frontiers in cellular and infection microbiology · 2020
    Review
  17. Role of iBALT in Respiratory Immunity.Current topics in microbiology and immunology · 2020
    Review
  18. A Common Variant ofDisease markers · 2019
    Article
  19. Review
  20. Review
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

2 authors at 1 institution in 1 country.

Lawton L RobertsDepartment of Pathology, Microbiology, & Immunology, University of South Carolina School of Medicine, Columbia, SC, USA.
Cory M Robinson
University of South Carolina · US

Funding

The involvement of IL-12 and IL-27 in immunity to Mycobacterium tuberculosisR00HL093300 · NHLBI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI ROBINSON, CORY MICHAEL · 2011 to 2013
$718k
The involvement of IL-12 and IL-27 in immunity to Mycobacterium tuberculosisK99HL093300 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ROBINSON, CORY MICHAEL · 2009 to 2010
$180k
NHLBI NIH HHS HL093300NHLBI NIH HHS K99 HL093300NHLBI NIH HHS R00 HL093300
6 · The paper itself

Abstract

Tuberculosis (TB) remains a major global health problem accounting for millions of deaths annually. Approximately one-third of the world's population is infected with the causative agent Mycobacterium tuberculosis. The onset of an adaptive immune response to M. tuberculosis is delayed compared with other microbial infections. This delay permits bacterial growth and dissemination. The precise mechanism(s) responsible for this delay have remained obscure. T-cell activation is preceded by dendritic cell (DC) migration from infected lungs to local lymph nodes and synapsis with T cells. We hypothesized that M. tuberculosis may impede the ability of DCs to reach lymph nodes and initiate an adaptive immune response. We used primary human DCs to determine the effect of M. tuberculosis on expression of heterodimeric integrins involved in cellular adhesion and migration. We also evaluated the ability of infected DCs to adhere to and migrate through lung endothelial cells, which is necessary to reach lymph nodes. We show by flow cytometry and confocal microscopy that M. tuberculosis-infected DCs exhibit a significant reduction in surface expression of the β(2) (CD18) integrin. Distribution of integrin β(2) is also markedly altered in M. tuberculosis-infected DCs. A corresponding reduction in the αL (CD11a) and αM (CD11b) subunits that associate with integrin β(2) was also observed. Consistent with reduced integrin surface expression, we show a significant reduction in adherence to lung endothelial cell monolayers and migration towards lymphatic chemokines when DCs are infected with M. tuberculosis. These findings suggest that M. tuberculosis modulates DC adhesion and migration to increase the time required to initiate an adaptive immune response.

Indexed as

AdolescentCell AdhesionCell MovementChemokinesDendritic CellsFemaleGene Expression RegulationHumansIntegrinsMaleMycobacterium tuberculosisTuberculosisChemokinesIntegrinsCD18dendritic cellsintegrinsmigrationmycobacteria

Identifiers

PMID23981064
PMCPMC3893848
OpenAlexW1984902805

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.