Evidence map›Paper›PMID 33202847›Full record

ArticleInternational journal of molecular sciences2020

TLR2 Deficiency Exacerbates Imiquimod-Induced Psoriasis-Like Skin Inflammation through Decrease in Regulatory T Cells and Impaired IL-10 Production.

Momoko Nakao, Makoto Sugaya, Hideki Fujita, Tomomitsu Miyagaki, Sohshi Morimura, Sayaka Shibata, Yoshihide Asano, Shinichi Sato

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. A review of core immuno-inflammatory mechanisms and key regulatory targets in psoriasis.American journal of clinical and experimental immunology · 2026
    Review
  4. Review
  5. Article
  6. Article
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  12. Article
  13. Article
  14. Suppression ofInternational journal of molecular sciences · 2022
    Article
  15. Novel Targeted Biological Agents for the Treatment of Atopic Dermatitis.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2021
    Review
  16. Review
  17. 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.

Momoko NakaoDepartment of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan.
Makoto SugayaDepartment of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan.ORCID 0000-0002-1618-329X
Hideki FujitaDepartment of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan.
Tomomitsu MiyagakiDepartment of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan.ORCID 0000-0003-1879-3128
Sohshi MorimuraDepartment of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan.
Sayaka ShibataDepartment of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan.
Yoshihide AsanoDepartment of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan.
Shinichi SatoDepartment of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan.
The University of Tokyo · JPNihon University · JPSt. Marianna University School of Medicine · JP

Funding

JSID's Fellowship SHISEIDO Research Grant. noneJSPS KAKENHI JP25461684Lydia O'leary Memorial Pias Dermatological Foundation none
6 · The paper itself

Abstract

Emerging evidence has demonstrated that Toll-like receptors (TLRs) are associated with autoimmune diseases. In this study, we investigated the role of TLR2 in psoriasis using imiquimod-induced psoriasis-like dermatitis. Although TLR2 signaling is known to play a critical role in the induction of proinflammatory cytokines by immune cells, such as dendritic cells (DCs), macrophages, and monocytes, TLR2 deficiency unexpectedly exacerbated psoriasiform skin inflammation. Importantly, messenger RNA (mRNA) levels of Foxp-3 and IL-10 in the lesional skin were significantly decreased in TLR2 KO mice compared with wild-type mice. Furthermore, flow cytometric analysis of the lymph nodes revealed that the frequency of regulatory T cells (Tregs) among CD4-positive cells was decreased. Notably, stimulation with Pam3CSK4 (TLR2/1 ligand) or Pam2CSK4 (TLR2/6 ligand) increased IL-10 production from Tregs and DCs and the proliferation of Tregs. Finally, adoptive transfer of Tregs from wild-type mice reduced imiquimod-induced skin inflammation in TLR2 KO mice. Taken together, our results suggest that TLR2 signaling directly enhances Treg proliferation and IL-10 production by Tregs and DCs, suppressing imiquimod-induced psoriasis-like skin inflammation. Enhancement of TLR2 signaling may be a new therapeutic strategy for psoriasis.

Indexed as

Interleukin-10PsoriasisSkinT-Lymphocytes, RegulatoryAnimalsImiquimodInflammationMiceMice, KnockoutToll-Like Receptor 2IL10 protein, mouseImiquimodInterleukin-10Tlr2 protein, mouseToll-Like Receptor 2dendritic cellsimiquimodpsoriasisregulatory T cellsTLR2

Identifiers

PMID33202847
PMCPMC7696365
OpenAlexW3104417068

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.