Evidence map›Paper›PMID 20524234›Full record

ReviewThe Journal of infectious diseases2010

Pathogenesis of genital tract disease due to Chlamydia trachomatis.

Toni Darville, Thomas J Hiltke

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of infectious diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed, 2 pooled it
17.1field-weighted citation impact, top 1% 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

185 citing papers in PubMed, 2 syntheses or guidelines pooled it, 329 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. HIV Transmission and Immunology of the Male Reproductive Tract.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Towards precision management ofFrontiers in cellular and infection microbiology · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Complete deletion of theInfection and immunity · 2025
    Article
  17. Article
  18. Article
  19. Article
  20. mSphere · 2025
    Article

125 more citing papers are in PubMed but not listed here.

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.

Toni DarvilleDepartments of Pediatrics and Immunology, University of Pittsburgh Medical Cente, USA.
Thomas J Hiltke
National Institutes of Health · US

Funding

The UPMC Sexually Transmitted Infections Cooperative Research CenterU19AI084024 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WIESENFELD, HAROLD C · 2009 to 2013
$12.9M
Cell Death and Innate Immunity in Chlamydial InfectionR01AI054624 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DARVILLE, TONI · 2003 to 2014
$3.2M
NIAID NIH HHS R01 AI054624NIAID NIH HHS U19 AI084024
6 · The paper itself

Abstract

Although the pathologic consequences of C. trachomatis genital infection are well-established, the mechanism(s)that result in chlamydia-induced tissue damage are not fully understood. We reviewed in vitro, animal, and human data related to the pathogenesis of chlamydial disease to better understand how reproductive sequelae result from C. trachomatis infection. Abundant in vitro data suggest that the inflammatory response to chlamydiae is initiated and sustained by actively infected nonimmune host epithelial cells. The mouse model indicates a critical role for chlamydia activation of the innate immune receptor, Toll-like receptor 2, and subsequent inflammatory cell influx and activation, which contributes to the development of chronic genital tract tissue damage. Data from recent vaccine studies in the murine model and from human immunoepidemiologic studies support a role for chlamydia-specific CD4 Th1-interferon-g-producing cells in protection from infection and disease. However, limited evidence obtained using animal models of repeated infection indicates that, although the adaptive T cell response is a key mechanism involved in controlling or eliminating infection, it may have a double-edged nature and contribute to tissue damage. Important immunologic questions include whether anamnestic CD4 T cell responses drive disease rather than protect against disease and the role of specific immune cells and inflammatory mediators in the induction of tissue damage with primary and repeated infections. Continued study of the complex molecular and cellular interactions between chlamydiae and their host and large-scale prospective immunoepidemiologic and immunopathologic studies are needed to address gaps in our understanding of pathogenesis that thwart development of optimally effective control programs, including vaccine development.

Indexed as

AnimalsChlamydia InfectionsChlamydia trachomatisDisease SusceptibilityEpithelial CellsHost-Pathogen InteractionsHumansImmunity, Cellular

Identifiers

PMID20524234
PMCPMC3150527
OpenAlexW2098304796

What OpenQuestion holds

Textmetadata
LicenceTDM
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.