Evidence map›Paper›PMID 28201690›Full record

ReviewFEMS microbiology reviews2016

Sensing the enemy, containing the threat: cell-autonomous immunity to Chlamydia trachomatis.

Ryan Finethy, Jörn Coers

Open access · bronzeAbstract readReview
In one paragraph

Review in FEMS microbiology reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. TheMicrobiology spectrum · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. The role of infected epithelial cells inFrontiers in cellular and infection microbiology · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Towards a Deeper Understanding ofInternational journal of molecular sciences · 2022
    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

2 authors at 1 institution in 1 country.

Ryan FinethyDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC, USA.
Jörn CoersDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC, USA.
Duke University Hospital · US

Funding

IRGM-driven host responses to Chlamydia trachomatis infectionsR01AI103197 · NIAID · DUKE UNIVERSITY · PI COERS, JOERN · 2013 to 2023
$4.2M
Interferon-inducible cell-intrinsic host defense against Chlamydia trachomatisR37AI103197 · NIAID · DUKE UNIVERSITY · PI Jorn Coers · 2024 to 2026
$1.6M
NIAID NIH HHS R37 AI103197
6 · The paper itself

Abstract

The bacterium Chlamydia trachomatis is the etiological agent of the most common sexually transmitted infection in North America and Europe. Medical complications resulting from genital C. trachomatis infections arise predominantly in women where the initial infections often remain asymptomatic and thus unrecognized. Untreated asymptomatic infections in women can ascend into the upper genital tract and establish persistence, ultimately resulting in extensive scarring of the reproductive organs, pelvic inflammatory disease, infertility and ectopic pregnancies. Previously resolved C. trachomatis infections fail to provide protective immune memory, and no effective vaccine against C. trachomatis is currently available. Critical determinants of the pathogenesis and immunogenicity of genital C. trachomatis infections are cell-autonomous immune responses. Cell-autonomous immunity describes the ability of an individual host cell to launch intrinsic immune circuits that execute the detection, containment and elimination of cell-invading pathogens. As an obligate intracellular pathogen C. trachomatis is constantly under attack by cell-intrinsic host defenses. Accordingly, C. trachomatis evolved to subvert and co-opt cell-autonomous immune pathways. This review will provide a critical summary of our current understanding of cell-autonomous immunity to C. trachomatis and its role in shaping host resistance, inflammation and adaptive immunity to genital C. trachomatis infections.

Indexed as

Models, ImmunologicalChlamydia InfectionsChlamydia trachomatisHumansInflammasomesToll-Like ReceptorsInflammasomesToll-Like ReceptorsChlamydia trachomatisindole-dioxygenaseinflammasomeinterferon-inducible GTPasesSTINGTLR

Identifiers

PMID28201690
PMCPMC5975928
OpenAlexW2483939470

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.