Evidence map›Paper›PMID 19228816›Full record

ArticleJournal of leukocyte biology2009

Murine dendritic cell antigen-presenting cell function is not altered by burn injury.

Satoshi Fujimi, Peter H Lapchak, Yan Zang, Malcolm P MacConmara, Adrian A Maung, Adam J Delisle, John A Mannick, James A Lederer

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Gp130-HIF1α axis-induced vascular damage is prevented by the short-term inhibition of IL-6 receptor signaling.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. High-Level Expression of Toll-Like Receptors on Dendritic Cells in Adult Patients with Burns on ≥90% of Total Body Surface Area (TBSA).Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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 1 country.

Satoshi FujimiDepartment of Surgery, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA.
Peter H Lapchak
Yan Zang
Malcolm P MacConmara
Adrian A Maung
Adam J Delisle
John A Mannick
James A Lederer
Brigham and Women's Hospital · USBeth Israel Deaconess Medical Center · USMassachusetts General Hospital · US

Funding

IMMUNOLOGIC STUDIES OF PATIENTS AFTER TRAUMATIC INJURYR01GM035633 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI LEDERER, JAMES A. · 1985 to 2010
$3.3M
INJURY-INDUCED EFFECTS ON THE ADAPTIVE IMMUNE SYSTEMR01GM057664 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI LEDERER, JAMES A. · 1999 to 2007
$2.6M
INJURY INDUCED EFFECTS ON THE ADAPTIVE IMMUNE SYSTEMR55GM057664 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI LEDERER, JAMES A. · 1998 to 1998
–
NIGMS NIH HHS GM35633NIGMS NIH HHS GM57664NIGMS NIH HHS R01 GM035633NIGMS NIH HHS R01 GM057664
6 · The paper itself

Abstract

Severe injury disrupts normal immune regulation causing a transient hyperinflammatory reaction and suppressed adaptive immune function. This report addresses the potential contribution of dendritic cells (DC) to changes in adaptive immune function after injury by specifically measuring injury-induced changes in splenic DC numbers and subsets, cell-surface markers, TLR responses, and APC function. Using a mouse burn injury model, we found that injury did not markedly alter the relative percentage of lymphoid, myeloid, or plasmacytoid DC in the spleens of burn-injured mice. Moreover, we did not observe a significant reduction in cell-surface expression of several major costimulatory molecules, CD40, CD80, CD86, programmed death 1 ligand, ICOS ligand, and B7-H3, on DC. Instead, we observed increased cell-surface expression of CD86 at 1 day after injury with no significant changes in costimulatory molecule expression at 7 days after injury, suggesting that burn injury causes an early activation of DC. In addition, injury did not suppress DC reactivity to TLR2, TLR4, or TLR9 agonists. Most important, DC prepared from injured mice were able to present peptide antigen to naive OTII TCR transgenic CD4+ T cells as efficiently and effectively as DC from sham-injured mice. We also found that CD4 T cells stimulated with antigen presented by DC from sham or burn mice showed similar levels of IL-2, IFN-gamma, IL-10, and IL-13 production. Taken together, these findings support the conclusion that DC do not acquire a suppressive phenotype following severe injury in mice.

Indexed as

AnimalsAntigen PresentationB7-2 AntigenBurnsCD4-Positive T-LymphocytesCytokinesDendritic CellsMiceMice, Inbred C57BLMice, TransgenicSpleenTh1 CellsTh2 CellsToll-Like ReceptorsB7-2 AntigenCytokinesToll-Like Receptors

Identifiers

PMID19228816
PMCPMC2669406
OpenAlexW2154972571

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.