Evidence map›Paper›PMID 25393765›Full record

ArticlePloS one2014

Progranulin facilitates conversion and function of regulatory T cells under inflammatory conditions.

Fanhua Wei, Yuying Zhang, Weiming Zhao, Xiuping Yu, Chuan-Ju Liu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

41 citing papers in PubMed, 55 citations in OpenAlex.

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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

5 authors at 2 institutions in 2 countries.

Fanhua WeiDepartment of Orthopaedic Surgery, New York University Medical Center, New York, New York, United States of America; Institute of Pathogenic Biology, Shandong University School of Medicine, Jinan, China.
Yuying ZhangDepartment of Orthopaedic Surgery, New York University Medical Center, New York, New York, United States of America.
Weiming ZhaoInstitute of Pathogenic Biology, Shandong University School of Medicine, Jinan, China.
Xiuping YuInstitute of Pathogenic Biology, Shandong University School of Medicine, Jinan, China.
Chuan-Ju LiuDepartment of Orthopaedic Surgery, New York University Medical Center, New York, New York, United States of America; Department of Cell Biology, New York University School of Medicine, New York, New York, United States of America.
Shandong University · CNNew York University · US

Funding

The immunological mechanism of PGRNs anti-inflammatory effect - Renewal - 1R01AR062207 · NIAMS · YALE UNIVERSITY · PI Chuanju Liu · 2012 to 2026
$5.6M
The Role of PGRN Growth Factor in Osteoarthritis. - Renewal - 1 - Revision - 2R01AR061484 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI LIU, CHUANJU · 2011 to 2020
$4.8M
Progranulin Intervention in Inflammatory Bowel DiseasesR56AI100901 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI LIU, CHUANJU · 2012 to 2013
$636k
NIAID NIH HHS R56 AI100901NIAID NIH HHS R56AI100901NIAMS NIH HHS R01 AR061484NIAMS NIH HHS R01AR061484NIAMS NIH HHS R01 AR062207NIAMS NIH HHS R01AR062207
6 · The paper itself

Abstract

The progranulin (PGRN) is known to protect regulatory T cells (Tregs) from a negative regulation by TNF-α, and its levels are elevated in various kinds of autoimmune diseases. Whether PGRN directly regulates the conversion of CD4+CD25-T cells into Foxp3-expressing regulatory T cells (iTreg), and whether PGRN affects the immunosuppressive function of Tregs, however, remain unknown. In this study we provide evidences demonstrating that PGRN is able to stimulate the conversion of CD4+CD25-T cells into iTreg in a dose-dependent manner in vitro. In addition, PGRN showed synergistic effects with TGF-β1 on the induction of iTreg. PGRN was required for the immunosuppressive function of Tregs, since PGRN-deficient Tregs have a significant decreased ability to suppress the proliferation of effector T cells (Teff). In addition, PGRN deficiency caused a marked reduction in Tregs number in the course of inflammatory arthritis, although no significant difference was observed in the numbers of Tregs between wild type and PGRN deficient mice during development. Furthermore, PGRN deficiency led to significant upregulation of the Wnt receptor gene Fzd2. Collectively, this study reveals that PGRN directly regulates the numbers and function of Tregs under inflammatory conditions, and provides new insight into the immune regulatory mechanism of PGRN in the pathogenesis of inflammatory and immune-related diseases.

Indexed as

AnimalsGranulinsImmune ToleranceInflammationIntercellular Signaling Peptides and ProteinsMiceProgranulinsT-Lymphocytes, RegulatoryTransforming Growth Factor beta1GranulinsGrn protein, mouseIntercellular Signaling Peptides and ProteinsProgranulinsTransforming Growth Factor beta1

Identifiers

PMID25393765
PMCPMC4230946
OpenAlexW2010258002

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.