Evidence map›Paper›PMID 31028244›Full record

ArticleExperimental & molecular medicine2019

A cell-penetrating peptide blocks Toll-like receptor-mediated downstream signaling and ameliorates autoimmune and inflammatory diseases in mice.

Hyuk-Kwon Kwon, Mahesh Chandra Patra, Hyeon-Jun Shin, Xiangai Gui, Asma Achek, Suresh Panneerselvam, Dong-Jin Kim, Suk-Jong Song, Riwon Hong, Kyoung Soo Kim and 5 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 37 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

15 authors at 4 institutions in 2 countries.

Hyuk-Kwon KwonDepartment of Molecular Science and Technology, Ajou University, Suwon, 16499, Korea.
Mahesh Chandra PatraDepartment of Molecular Science and Technology, Ajou University, Suwon, 16499, Korea.ORCID http://orcid.org/0000-0003-0471-6236
Hyeon-Jun ShinDepartment of Molecular Science and Technology, Ajou University, Suwon, 16499, Korea.
Xiangai GuiDepartment of Molecular Science and Technology, Ajou University, Suwon, 16499, Korea.
Asma AchekDepartment of Molecular Science and Technology, Ajou University, Suwon, 16499, Korea.
Suresh PanneerselvamDepartment of Molecular Science and Technology, Ajou University, Suwon, 16499, Korea.
Dong-Jin KimDivision of Nephrology, Department of Internal Medicine, Kyung Hee University Hospital at Gangdong, Seoul, 05278, Korea.
Suk-Jong SongDivision of Nephrology, Department of Internal Medicine, Kyung Hee University Hospital at Gangdong, Seoul, 05278, Korea.
Riwon HongDepartment of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Korea.
Kyoung Soo KimEast-West Bone & Joint Research Institute, Kyung Hee University Hospital at Gangdong, Seoul, 05278, Korea.
Yang Gyun KimDivision of Nephrology, Department of Internal Medicine, Kyung Hee University Hospital at Gangdong, Seoul, 05278, Korea.
Francis Y LeeDepartment of Orthopaedics and Rehabilitation, Yale School of Medicine, New Haven, CT, 06510, USA.
Dae-Hyun HahmDepartment of Physiology, School of Medicine, Kyung Hee University, Seoul, 02447, Korea.
Sang Ho LeeDivision of Nephrology, Department of Internal Medicine, Kyung Hee University Hospital at Gangdong, Seoul, 05278, Korea.
Sangdun ChoiDepartment of Molecular Science and Technology, Ajou University, Suwon, 16499, Korea. sangdunchoi@ajou.ac.kr.
Ajou University · KRKyung Hee University Hospital at Gangdong · KRKyung Hee University · KRYale University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007205 · NIGMS · YALE UNIVERSITY · PI KAZMIERCZAK, BARBARA I · 1985 to 2019
$42.9M
National Research Foundation of Korea (NRF) NRF-2015R1A2A2A09001059NIGMS NIH HHS T32 GM007205
6 · The paper itself

Abstract

Toll-like receptors (TLRs) recognize pathogen/damage-associated molecular patterns and initiate inflammatory signaling cascades. Occasionally, overexpression of TLRs leads to the onset of numerous inflammatory diseases, necessitating the development of selective inhibitors to allow a protective yet balanced immune response. Here, we demonstrate that a novel peptide (TIP1) derived from Toll/interleukin-1 receptor (TIR) domain-containing adapter protein inhibited multiple TLR signaling pathways (MyD88-dependent and MyD88-independent) in murine and human cell lines. TIP1 also inhibited NLRP3-mediated IL-1β secretion, as we validated at both the protein and mRNA levels. Biophysical experiments confirmed that TIP1 specifically binds to the BB loop of the TLR4-TIR domain. Animal studies revealed that TIP1 inhibited the secretion of lipopolysaccharide (LPS)-induced proinflammatory cytokines in collagen-induced arthritis (CIA) and kaolin/carrageenan-induced arthritis (K/C) rodent models. TIP1 also rescued animals from sepsis and from LPS-induced kidney/liver damage. Importantly, TIP1 ameliorated the symptoms of rheumatoid arthritis in CIA and K/C rodent models, suggesting that TIP1 has therapeutic potential for the treatment of TLR-mediated autoimmune/inflammatory diseases.

Indexed as

AnimalsBlotting, WesternCell SurvivalInterferon-betaInterleukin-1betaMaleMiceMice, Inbred BALB CMice, Inbred C57BLMicroscopy, ConfocalPeptidesRats, Sprague-DawleyRAW 264.7 CellsSignal TransductionToll-Like Receptor 4Toll-Like ReceptorsInterferon-betaInterleukin-1betaPeptidesToll-Like Receptor 4Toll-Like Receptors

Identifiers

PMID31028244
PMCPMC6486608
OpenAlexW2942075504

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.