Evidence map›Paper›PMID 20625513›Full record

ArticlePloS one2010

Dendritic cells in chronic mycobacterial granulomas restrict local anti-bacterial T cell response in a murine model.

Heidi A Schreiber, Paul D Hulseberg, JangEun Lee, Jozsef Prechl, Peter Barta, Nora Szlavik, Jeffrey S Harding, Zsuzsanna Fabry, Matyas Sandor

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
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  4. Review
  5. The Roles of Inflammasomes in Host Defense againstPathogens (Basel, Switzerland) · 2021
    Review
  6. Immunomodulatory Effects of RecombinantPathogens (Basel, Switzerland) · 2020
    Article
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  9. Article
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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 3 institutions in 2 countries.

Heidi A SchreiberDepartment of Pathology and Laboratory Medicine, University of Wisconsin, School of Medicine and Public Health, Madison, Wisconsin, United States of America.
Paul D Hulseberg
JangEun Lee
Jozsef Prechl
Peter Barta
Nora Szlavik
Jeffrey S Harding
Zsuzsanna Fabry
Matyas Sandor
University of Wisconsin–Madison · USBajcsy-Zsilinszky Kórház és Rendelőintézet · HUSemmelweis University · HU

Funding

ANTIGEN SPECIFIC T CELL ACCUMULATION IN THE CNSR01NS037570 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2000 to 2012
$3.1M
Antigen specific T cell accumulation in the CNSR56NS037570 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2008 to 2008
$367k
NINDS NIH HHS R01 NS037570NINDS NIH HHS R56 NS037570PHS HHS R01-A1048087PHS HHS R21-A1072638
6 · The paper itself

Abstract

backgroundMycobacterium-induced granulomas are the interface between bacteria and host immune response. During acute infection dendritic cells (DCs) are critical for mycobacterial dissemination and activation of protective T cells. However, their role during chronic infection in the granuloma is poorly understood. METHODOLOGY/PRINCIPAL

findingsWe report that an inflammatory subset of murine DCs are present in granulomas induced by Mycobacteria bovis strain Bacillus Calmette-guerin (BCG), and both their location in granulomas and costimulatory molecule expression changes throughout infection. By flow cytometric analysis, we found that CD11c(+) cells in chronic granulomas had lower expression of MHCII and co-stimulatory molecules CD40, CD80 and CD86, and higher expression of inhibitory molecules PD-L1 and PD-L2 compared to CD11c(+) cells from acute granulomas. As a consequence of their phenotype, CD11c(+) cells from chronic lesions were unable to support the reactivation of newly-recruited, antigen 85B-specific CD4(+)IFNgamma(+) T cells or induce an IFNgamma response from naïve T cells in vivo and ex vivo. The mechanism of this inhibition involves the PD-1:PD-L signaling pathway, as ex vivo blockade of PD-L1 and PD-L2 restored the ability of isolated CD11c(+) cells from chronic lesions to stimulate a protective IFNgamma T cell response. CONCLUSIONS/SIGNIFICANCE: Our data suggest that DCs in chronic lesions may facilitate latent infection by down-regulating protective T cell responses, ultimately acting as a shield that promotes mycobacterium survival. This DC shield may explain why mycobacteria are adapted for long-term survival in granulomatous lesions.

Indexed as

AnimalsAntigens, BacterialAntigens, CDB7-1 AntigenB7-2 AntigenB7-H1 AntigenCD11c AntigenCD40 AntigensCD4-Positive T-LymphocytesCells, CulturedDendritic CellsFlow CytometryGranulomaIntercellular Signaling Peptides and ProteinsInterferon-gammaMiceAntigens, BacterialAntigens, CDB7-1 AntigenB7-2 AntigenB7-H1 AntigenCD11c AntigenCD274 protein, humanCD40 AntigensIntercellular Signaling Peptides and ProteinsInterferon-gammaPDCD1LG2 protein, humanPdcd1lg2 protein, mouseProgrammed Cell Death 1 Ligand 2 Protein

Identifiers

PMID20625513
PMCPMC2897891
OpenAlexW2040289165

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.