Evidence map›Paper›PMID 11083777›Full record

ArticleInfection and immunity2000

Bacterial pathogens induce abscess formation by CD4(+) T-cell activation via the CD28-B7-2 costimulatory pathway.

A O Tzianabos, A Chandraker, W Kalka-Moll, F Stingele, V M Dong, R W Finberg, R Peach, M H Sayegh

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 51 citations in OpenAlex.

  1. From the Friend to the Foe-International journal of molecular sciences · 2024
    Review
  2. Review
  3. Pathogenic potential ofBMJ case reports · 2020
    Article
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  20. CD4+ T cells and CXC chemokines modulate the pathogenesis of Staphylococcus aureus wound infections.Proceedings of the National Academy of Sciences of the United States of America · 2006
    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

8 authors at 3 institutions in 2 countries.

A O TzianabosChanning Laboratory, Department of Medicine, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA. atzianabos@channing.harvard.edu
A Chandraker
W Kalka-Moll
F Stingele
V M Dong
R W Finberg
R Peach
M H Sayegh
Brigham and Women's Hospital · USBristol-Myers Squibb (Sweden) · SEDana-Farber Cancer Institute · US

Funding

PATHOGENIC MECHANISMS OF ANAEROBES IN SEPSISR01AI039576 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI KASPER, DENNIS L. · 1997 to 2007
$2.4M
INTRATHYMIC TRANSPLANTATION TOLERANCE BY MHC PEPTIDESR01AI034965 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI SAYEGH, MOHAMED H · 1999 to 2003
$1.3M
PATHOGENIC MECHANISMS OF ANAEROBES IN SEPSISR21AI039576 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI KASPER, DENNIS L. · 1996 to 1996
–
BACTEROIDES FRAGILIS CAPSULES--SYNTHESIS AND VIRULENCER29AI034073 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI TZIANABOS, ARTHUR O · 1995 to 1999
–
INTRATHYMIC TRANSPLANTATION TOLERANCE BY MHC PEPTIDESR29AI034965 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI SAYEGH, MOHAMED H · 1994 to 1998
–
NIAID NIH HHS AI 34073NIAID NIH HHS AI 34965NIAID NIH HHS AI 39576NIAID NIH HHS R01 AI034965NIAID NIH HHS R01 AI039576
6 · The paper itself

Abstract

Abscesses are a classic host response to infection by many pathogenic bacteria. The immunopathogenesis of this tissue response to infection has not been fully elucidated. Previous studies have suggested that T cells are involved in the pathologic process, but the role of these cells remains unclear. To delineate the mechanism by which T cells mediate abscess formation associated with intra-abdominal sepsis, the role of T-cell activation and the contribution of antigen-presenting cells via CD28-B7 costimulation were investigated. T cells activated in vitro by zwitterionic bacterial polysaccharides (Zps) known to induce abscess formation required CD28-B7 costimulation and, when adoptively transferred to the peritoneal cavity of naïve rats, promoted abscess formation. Blockade of T-cell activation via the CD28-B7 pathway in animals with CTLA4Ig prevented abscess formation following challenge with different bacterial pathogens, including Staphylococcus aureus, Bacteroides fragilis, and a combination of Enterococcus faecium and Bacteroides distasonis. In contrast, these animals had an increased abscess rate following in vivo T-cell activation via CD28 signaling. Abscess formation in vivo and T-cell activation in vitro required costimulation by B7-2 but not B7-1. These results demonstrate that abscess formation by pathogenic bacteria is under the control of a common effector mechanism that requires T-cell activation via the CD28-B7-2 pathway.

Indexed as

ImmunoconjugatesLymphocyte ActivationAbataceptAbscessAnimalsAntigens, CDAntigens, DifferentiationB7-1 AntigenB7-2 AntigenCD28 AntigensCD4-Positive T-LymphocytesCTLA-4 AntigenHumansMaleMembrane GlycoproteinsRatsAbataceptAntigens, CDAntigens, DifferentiationB7-1 AntigenB7-2 AntigenCD28 AntigensCD86 protein, humanCd86 protein, ratCTLA-4 AntigenCTLA4 protein, humanCtla4 protein, ratImmunoconjugatesMembrane Glycoproteins

Identifiers

PMID11083777
PMCPMC97762
OpenAlexW2119524661

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.