Evidence map›Paper›PMID 21536799›Full record

ArticleInfection and immunity2011

Tumor necrosis factor alpha production from CD8+ T cells mediates oviduct pathological sequelae following primary genital Chlamydia muridarum infection.

Ashlesh K Murthy, Weidang Li, Bharat K R Chaganty, Sangamithra Kamalakaran, M Neal Guentzel, J Seshu, Thomas G Forsthuber, Guangming Zhong, Bernard P Arulanandam

Abstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 140 citations in OpenAlex.

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  17. Frontiers in cell and developmental biology · 2024
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  20. Plasmid-mediated virulence inFrontiers in cellular and infection microbiology · 2023
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44 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

9 authors at 2 institutions in 1 country.

Ashlesh K MurthySouth Texas Center for Emerging Infectious Diseases, Department of Biology, University of Texas at San Antonio, San Antonio, Texas 78249, USA. Ashlesh.murthy@utsa.edu
Weidang Li
Bharat K R Chaganty
Sangamithra Kamalakaran
M Neal Guentzel
J Seshu
Thomas G Forsthuber
Guangming Zhong
Bernard P Arulanandam
Texas Center for Infectious Disease · USThe University of Texas Health Science Center at San Antonio · US

Funding

CPAF induced CD4+ T cell mediated immunity against ChlamydiaR01AI074860 · NIAID · UNIVERSITY OF TEXAS SAN ANTONIO · PI ARULANANDAM, BERNARD PRAGASH · 2009 to 2013
$1.9M
Role of CD8+ T cells in Reproductive Sequelae Induced by Chlamydia InfectionR03AI088342 · NIAID · UNIVERSITY OF TEXAS SAN ANTONIO · PI MURTHY, ASHLESH KRISHNA · 2010 to 2011
$144k
NIAID NIH HHS 1R01AI074860NIAID NIH HHS 1R03AI088342NIAID NIH HHS R01 AI074860NIAID NIH HHS R03 AI088342
6 · The paper itself

Abstract

The immunopathogenesis of Chlamydia trachomatis-induced oviduct pathological sequelae is not well understood. Mice genetically deficient in perforin (perforin(-/-) mice) or tumor necrosis factor alpha (TNF-α) production (TNF-α(-/-) mice) displayed comparable vaginal chlamydial clearance rates but significantly reduced oviduct pathology (hydrosalpinx) compared to that of wild-type mice. Since both perforin and TNF-α are effector mechanisms of CD8(+) T cells, we evaluated the role of CD8(+) T cells during genital Chlamydia muridarum infection and oviduct sequelae. Following vaginal chlamydial challenge, (i) mice deficient in TAP I (and therefore the major histocompatibility complex [MHC] I pathway and CD8(+) T cells), (ii) wild-type mice depleted of CD8(+) T cells, and (iii) mice genetically deficient in CD8 (CD8(-/-) mice) all displayed similar levels of vaginal chlamydial clearance but significantly reduced hydrosalpinx, compared to those of wild-type C57BL/6 mice, suggesting a role for CD8(+) T cells in chlamydial pathogenesis. Repletion of CD8(-/-) mice with wild-type or perforin(-/-), but not TNF-α(-/-), CD8(+) T cells at the time of challenge restored hydrosalpinx to levels observed in wild-type C57BL/6 mice, suggesting that TNF-α production from CD8(+) T cells is important for pathogenesis. Additionally, repletion of TNF-α(-/-) mice with TNF-α(+/+) CD8(+) T cells significantly enhanced the incidence of hydrosalpinx and oviduct dilatation compared to those of TNF-α(-/-) mice but not to the levels found in wild-type mice, suggesting that TNF-α production from CD8(+) T cells and non-CD8(+) cells cooperates to induce optimal oviduct pathology following genital chlamydial infection. These results provide compelling new evidence supporting the contribution of CD8(+) T cells and TNF-α production to Chlamydia-induced reproductive tract sequelae.

Indexed as

Chlamydia muridarumAnimalsCD8-Positive T-LymphocytesChlamydia InfectionsFallopian TubesFemaleGenital Diseases, FemaleHeLa CellsHumansMiceMice, Inbred C57BLMice, KnockoutPerforinTumor Necrosis Factor-alphaVaginaPerforinTumor Necrosis Factor-alpha

Identifiers

PMID21536799
PMCPMC3191981
OpenAlexW2131485868

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.