Evidence map›Paper›PMID 28539427›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

TLR-Induced Murine Dendritic Cell (DC) Activation Requires DC-Intrinsic Complement.

Joong-Hyuk Sheen, Michael G Strainic, Jinbo Liu, Weijia Zhang, Zhengzi Yi, M Edward Medof, Peter S Heeger

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

46 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Complement activation in kidney transplantation.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Review
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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

7 authors at 2 institutions in 1 country.

Joong-Hyuk SheenDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029.ORCID 0000-0002-1855-0268
Michael G StrainicInstitute of Pathology, Case Western Reserve University, Cleveland, OH 44106.ORCID 0000-0003-2438-8540
Jinbo LiuInstitute of Pathology, Case Western Reserve University, Cleveland, OH 44106.
Weijia ZhangDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Zhengzi YiDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
M Edward MedofInstitute of Pathology, Case Western Reserve University, Cleveland, OH 44106 peter.heeger@mssm.edu mxm16@case.edu.
Peter S HeegerDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029; peter.heeger@mssm.edu mxm16@case.edu.ORCID 0000-0003-4673-6913
Icahn School of Medicine at Mount Sinai · USCase Western Reserve University · US

Funding

Complement & T Cell Medicated Allograft RejectionR01AI071185 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HEEGER, PETER SCOTT · 2007 to 2016
$4.3M
NIAID NIH HHS R01 AI071185
6 · The paper itself

Abstract

Induction of proinflammatory T cell immunity is augmented by innate dendritic cell (DC) maturation commonly initiated by TLR signaling. We demonstrate that ligation of TLR3, TLR4, and TLR9 induces murine DC production of complement components and local production of the anaphylatoxin C5a. In vitro, ex vivo, and in vivo analyses show that TLR-induced DC maturation, as assessed by surface phenotype, expression profiling by gene array, and functional ability to stimulate T cell responses, requires autocrine C3a receptor and C5a receptor (C3ar1/C5ar1) signaling. Studies using bone marrow chimeric animals and Foxp3-GFP/ERT2-Cre/dTomato fate-mapping mice show that TLR-initiated DC autocrine C3ar1/C5ar1 signaling causes expansion of effector T cells and instability of regulatory T cells and contributes to T cell-dependent transplant rejection. Together, our data position immune cell-derived complement production and autocrine/paracrine C3ar1/C5ar1 signaling as crucial intermediary processes that link TLR stimulation to DC maturation and the subsequent development of effector T cell responses.

Indexed as

AnimalsCell DifferentiationCells, CulturedComplement C3aComplement C5aDendritic CellsMiceSignal TransductionT-Lymphocytes, RegulatoryToll-Like Receptor 3Toll-Like Receptor 4Toll-Like Receptor 9Complement C3aComplement C5aTLR3 protein, mouseTlr4 protein, mouseTlr9 protein, mouseToll-Like Receptor 3Toll-Like Receptor 4Toll-Like Receptor 9

Identifiers

PMID28539427
PMCPMC5609833
OpenAlexW2618245942

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.