Evidence map›Paper›PMID 28652396›Full record

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

TLR7 Signaling Regulates Th17 Cells and Autoimmunity: Novel Potential for Autoimmune Therapy.

Jian Ye, Yadan Wang, Xia Liu, Lingyun Li, Adeleye Opejin, Eddy C Hsueh, Huanle Luo, Tian Wang, Daniel Hawiger, Guangyong Peng

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 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 35 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

10 authors at 2 institutions in 1 country.

Jian YeDivision of Infectious Diseases, Allergy, and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, MO 63104.ORCID 0000-0002-6955-9262
Yadan WangDivision of Infectious Diseases, Allergy, and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, MO 63104.
Xia LiuDivision of Infectious Diseases, Allergy, and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, MO 63104.
Lingyun LiDivision of Infectious Diseases, Allergy, and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, MO 63104.
Adeleye OpejinDepartment of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO 63104.
Eddy C HsuehDivision of General Surgery, Department of Surgery, Saint Louis University School of Medicine, St. Louis, MO 63110; and.
Huanle LuoDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555.
Tian WangDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555.
Daniel HawigerDepartment of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO 63104.
Guangyong PengDivision of Infectious Diseases, Allergy, and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, MO 63104; gpeng@slu.edu.
Saint Louis University · USThe University of Texas Medical Branch at Galveston · US

Funding

Gamma/Delta Treg Cells and Human Breast CancerR01CA184379 · NCI · SAINT LOUIS UNIVERSITY · PI PENG, GUANGYONG · 2015 to 2019
$1.7M
T Regulatory Cells and Neonatal Innate ImmunityR21AI094478 · NIAID · SAINT LOUIS UNIVERSITY · PI KOENIG, JOYCE MARIE, PENG, GUANGYONG · 2012 to 2013
$413k
Commitment and Plasticity of Th17 cells and Tregs in the Tumor MicroenvironmentR21AI097852 · NIAID · SAINT LOUIS UNIVERSITY · PI PENG, GUANGYONG · 2012 to 2013
$413k
NCI NIH HHS R01 CA184379NIAID NIH HHS R21 AI094478NIAID NIH HHS R21 AI097852
6 · The paper itself

Abstract

Innate regulation through TLR signaling has been shown to be important for promoting T cell subset development and function. However, limited information is known about whether differential TLR signaling can selectively inhibit Th17 and/or Th1 cells, which are important for controlling excessive inflammation and autoimmune responses. In this article, we demonstrate that activation of TLR7 signaling in T cells can inhibit Th17 cell differentiation from naive T cells and IL-17 production in established Th17 cells. We further report that downregulation of STAT3 signaling is responsible for TLR7-mediated inhibition of Th17 cells due to induction of suppressor of cytokine signaling 3 and 5. TLR7-mediated suppression of Th17 cells does not require dendritic cell involvement. In addition, we show that TLR7 signaling can suppress Th1 cell development and function through a mechanism different from Th17 cell suppression. Importantly, our complementary in vivo studies demonstrate that treatment with the TLR7 ligand imiquimod can inhibit Th1 and Th17 cells, resulting in the prevention of, and an immunotherapeutic reduction in, experimental autoimmune encephalomyelitis. These studies identify a new strategy to manipulate Th17/Th1 cells through TLR7 signaling, with important implications for successful immunotherapy against autoimmune and inflammatory diseases.

Indexed as

AminoquinolinesAnimalsAutoimmunityCell DifferentiationDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalHumansImiquimodImmunotherapyInflammationInterleukin-17Membrane GlycoproteinsMiceSignal TransductionSTAT3 Transcription FactorSuppressor of Cytokine Signaling ProteinsAminoquinolinesImiquimodInterleukin-17Membrane GlycoproteinsSTAT3 Transcription FactorSuppressor of Cytokine Signaling ProteinsTLR7 protein, humanTlr7 protein, mouseToll-Like Receptor 7

Identifiers

PMID28652396
PMCPMC5542577
OpenAlexW2731192412

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.