Evidence map›Paper›PMID 16254597›Full record

ArticlePLoS pathogens2005

Anthrax lethal toxin-mediated killing of human and murine dendritic cells impairs the adaptive immune response.

Abdelkrim Alileche, Evan R Serfass, Stefan M Muehlbauer, Steven A Porcelli, Jürgen Brojatsch

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Advances in structure determination by cryo-EM to unravel membrane-spanning pore formation.Protein science : a publication of the Protein Society · 2018
    Review
  5. Article
  6. Review
  7. Article
  8. Caspase-1 autoproteolysis is differentially required for NLRP1b and NLRP3 inflammasome function.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  9. Article
  10. Article
  11. Article
  12. Cellular and physiological effects of anthrax exotoxin and its relevance to disease.Frontiers in cellular and infection microbiology · 2012
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 3 institutions in 1 country.

Abdelkrim AlilecheDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York, USA.
Evan R Serfass
Stefan M Muehlbauer
Steven A Porcelli
Jürgen Brojatsch
Albert Einstein College of Medicine · USYeshiva University · USGeorgetown University · US

Funding

Viral Pathogenesis and TherapeuticsU54AI057158 · NIAID · WADSWORTH CENTER · PI LIPKIN, W. IAN · 2003 to 2014
$100.8M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
"The Tuberculous Granuloma"P01AI063537 · NIAID · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI CHAN, JOHN R. · 2005 to 2015
$15.7M
NIAID NIH HHS P01 AI063537NIAID NIH HHS U54 AI057158NIGMS NIH HHS T32 GM007288
6 · The paper itself

Abstract

Many pathogens have acquired strategies to combat the immune response. Bacillus anthracis interferes with host defenses by releasing anthrax lethal toxin (LT), which inactivates mitogen-activated protein kinase pathways, rendering dendritic cells (DCs) and T lymphocytes nonresponsive to immune stimulation. However, these cell types are considered resistant to killing by LT. Here we show that LT kills primary human DCs in vitro, and murine DCs in vitro and in vivo. Kinetics of LT-mediated killing of murine DCs, as well as cell death pathways induced, were dependent upon genetic background: LT triggered rapid necrosis in BALB/c-derived DCs, and slow apoptosis in C57BL/6-derived DCs. This is consistent with rapid and slow killing of LT-injected BALB/c and C57BL/6 mice, respectively. We present evidence that anthrax LT impairs adaptive immunity by specifically targeting DCs. This may represent an immune-evasion strategy of the bacterium, and contribute to anthrax disease progression. We also established that genetic background determines whether apoptosis or necrosis is induced by LT. Finally, killing of C57BL/6-derived DCs by LT mirrors that of human DCs, suggesting that C57BL/6 DCs represent a better model system for human anthrax than the prototypical BALB/c macrophages.

Identifiers

PMID16254597
PMCPMC1266308
OpenAlexW2145742637

What OpenQuestion holds

Textmetadata
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.