Evidence map›Paper›PMID 32369443›Full record

ArticleJCI insight2020

Mycobacterium tuberculosis cords within lymphatic endothelial cells to evade host immunity.

Thomas R Lerner, Christophe J Queval, Rachel P Lai, Matthew Rg Russell, Antony Fearns, Daniel J Greenwood, Lucy Collinson, Robert J Wilkinson, Maximiliano G Gutierrez

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
0.8field-weighted citation impact, top 16% 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

34 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Host- and pathogen-related determinants of pulmonaryEuropean respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Autophagy and Bacterial infections.Autophagy reports · 2025
    Review
  15. Article
  16. Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. MedComm · 2023
    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

9 authors at 3 institutions in 4 countries.

Thomas R LernerHost-pathogen interactions in tuberculosis laboratory.
Christophe J QuevalHost-pathogen interactions in tuberculosis laboratory.
Rachel P LaiTuberculosis laboratory, and.
Matthew Rg RussellElectron Microscopy Scientific Technology Platform, The Francis Crick Institute, London, United Kingdom.
Antony FearnsHost-pathogen interactions in tuberculosis laboratory.
Daniel J GreenwoodHost-pathogen interactions in tuberculosis laboratory.
Lucy CollinsonElectron Microscopy Scientific Technology Platform, The Francis Crick Institute, London, United Kingdom.
Robert J WilkinsonTuberculosis laboratory, and.
Maximiliano G GutierrezHost-pathogen interactions in tuberculosis laboratory.
Interactions hôtes-agents pathogènes · FRNational Tuberculosis Institute · INThe Francis Crick Institute · GB

Funding

Cancer Research UK FC001092Cancer Research UK FC00110218Medical Research Council FC001092Medical Research Council FC00110218Medical Research Council MR/R008922/1Wellcome Trust 104803Wellcome Trust 203135Wellcome Trust FC001092Wellcome Trust FC00110218
6 · The paper itself

Abstract

The ability of Mycobacterium tuberculosis to form serpentine cords is intrinsically related to its virulence, but specifically how M. tuberculosis cording contributes to pathogenesis remains obscure. Here, we show that several M. tuberculosis clinical isolates form intracellular cords in primary human lymphatic endothelial cells (hLECs) in vitro and in the lymph nodes of patients with tuberculosis. We identified via RNA-Seq a transcriptional program that activated, in infected-hLECs, cell survival and cytosolic surveillance of pathogens pathways. Consistent with this, cytosolic access was required for intracellular M. tuberculosis cording. Mycobacteria lacking ESX-1 type VII secretion system or phthiocerol dimycocerosates expression, which failed to access the cytosol, were indeed unable to form cords within hLECs. Finally, we show that M. tuberculosis cording is a size-dependent mechanism used by the pathogen to avoid its recognition by cytosolic sensors and evade either resting or IFN-γ-induced hLEC immunity. These results explain the long-standing association between M. tuberculosis cording and virulence and how virulent mycobacteria use intracellular cording as strategy to successfully adapt and persist in the lymphatic tracts.

Indexed as

Antigens, BacterialBacterial ProteinsEndothelial CellsImmune EvasionMycobacterium tuberculosisTuberculosisVirulence FactorsCells, CulturedHumansInterferon-gammaRNA-SeqAntigens, BacterialBacterial ProteinsESAT-6 protein, Mycobacterium tuberculosisIFNG protein, humanInterferon-gammaVirulence FactorsBacterial infectionsInfectious diseaseLymphLysosomesVascular Biology

Identifiers

PMID32369443
PMCPMC7259532
OpenAlexW3023347597

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.