Evidence map›Paper›PMID 22253566›Full record

ReviewInternational journal of biological sciences2012

The pro-inflammatory role of TGFβ1: a paradox?

Gangwen Han, Fulun Li, Tej Pratap Singh, Peter Wolf, Xiao-Jing Wang

Open access · goldAbstract readReview
In one paragraph

Review in International journal of biological sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

71 citing papers in PubMed, 153 citations in OpenAlex.

  1. Dietary Intake ofNutrients · 2021
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  14. The Expression ofInternational journal of molecular sciences · 2023
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11 more citing papers are in PubMed but not listed here.

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.

Gangwen HanDepartment of Pathology, University of Colorado Denver, Aurora, CO 80045, USA.
Fulun Li
Tej Pratap Singh
Peter Wolf
Xiao-Jing Wang
University of Colorado Denver · USShanghai University of Traditional Chinese Medicine · CN

Funding

Role of TGFbeta signaling in HNSCC progressionR01DE015953 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI WANG, XIAO-JING · 2004 to 2014
$3.6M
Effects of Altering TGF Beta Signaling on Wound HealingR01AR061792 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI WANG, XIAO-JING · 2011 to 2015
$1.9M
NCI NIH HHS CA80849NIAMS NIH HHS AR061792NIAMS NIH HHS R01 AR061792NIDCR NIH HHS DE15953NIDCR NIH HHS R01 DE015953
6 · The paper itself

Abstract

TGFβ1 was initially identified as a potent chemotactic cytokine to initiate inflammation, but the autoimmune phenotype seen in TGFβ1 knockout mice reversed the dogma of TGFβ1 being a pro-inflammatory cytokine to predominantly an immune suppressor. The discovery of the role of TGFβ1 in Th17 cell activation once again revealed the pro-inflammatory effect of TGFβ1. We developed K5.TGFβ1 mice with latent human TGFβ1 overexpression targeted to epidermal keratinocytes by keratin 5. These transgenic mice developed significant skin inflammation. Further studies revealed that inflammation severity correlated with switching TGFβ1 transgene expression on and off, and genome wide expression profiling revealed striking similarities between K5.TGFβ1 skin and human psoriasis, a Th1/Th17-associated inflammatory skin disease. Our recent study reveals that treatments alleviating inflammatory skin phenotypes in this mouse model reduced Th17 cells, and antibodies against IL-17 also lessen the inflammatory phenotype. Examination of inflammatory cytokines/chemokines affected by TGFβ1 revealed predominantly Th1-, Th17-related cytokines in K5.TGFβ1 skin. However, the finding that K5.TGFβ1 mice also express Th2-associated inflammatory cytokines under certain pathological conditions raises the possibility that deregulated TGFβ signaling is involved in more than one inflammatory disease. Furthermore, activation of both Th1/Th17 cells and regulatory T cells (Tregs) by TGFβ1 reversely regulated by IL-6 highlights the dual role of TGFβ1 in regulating inflammation, a dynamic, context and organ specific process. This review focuses on the role of TGFβ1 in inflammatory skin diseases.

Indexed as

AnimalsGene Expression ProfilingHumansLymphocyte ActivationMiceMice, TransgenicModels, ImmunologicalPsoriasisTh17 CellsTransforming Growth Factor beta1Transforming Growth Factor beta1skin inflammationTGFβ1

Identifiers

PMID22253566
PMCPMC3258562
OpenAlexW2133838032

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.