Evidence map›Paper›PMID 30800133›Full record

ArticleFrontiers in immunology2019

Specific Inhibition of Soluble γc Receptor Attenuates Collagen-Induced Arthritis by Modulating the Inflammatory T Cell Responses.

Byunghyuk Lee, Yuna Jo, Geona Kim, Laraib Amir Ali, Dong Hyun Sohn, Seung-Geun Lee, Kiseok Kim, Euisu Shin, Sung Ho Ryu, Changwan Hong

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

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  12. CD4Frontiers in immunology · 2019
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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 3 institutions in 1 country.

Byunghyuk LeeDepartment of Anatomy, Pusan National University School of Medicine, Yangsan, South Korea.
Yuna JoDepartment of Anatomy, Pusan National University School of Medicine, Yangsan, South Korea.
Geona KimDepartment of Anatomy, Pusan National University School of Medicine, Yangsan, South Korea.
Laraib Amir AliDepartment of Anatomy, Pusan National University School of Medicine, Yangsan, South Korea.
Dong Hyun SohnDepartment of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, South Korea.
Seung-Geun LeeDivision of Rheumatology, Department of Internal Medicine, Pusan National University School of Medicine, Pusan National University Hospital, Busan, South Korea.
Kiseok KimAptamer Sciences Inc., POSTECH Biotech Center, Pohang, South Korea.
Euisu ShinAptamer Sciences Inc., POSTECH Biotech Center, Pohang, South Korea.
Sung Ho RyuDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, South Korea.
Changwan HongDepartment of Anatomy, Pusan National University School of Medicine, Yangsan, South Korea.
Pusan National University · KRPohang University of Science and Technology · KRPusan National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-17 produced by Th17 cells has been implicated in the pathogenesis of rheumatoid arthritis (RA). It is important to prevent the differentiation of Th17 cells in RA. Homodimeric soluble γc (sγc) impairs IL-2 signaling and enhances Th17 differentiation. Thus, we aimed to block the functions of sγc by inhibiting the formation of homodimeric sγc. The homodimeric form of sγc was strikingly disturbed by sγc-binding DNA aptamer. Moreover, the aptamer effectively inhibited Th17 cell differentiation and restored IL-2 and IL-15 signaling impaired by sγc with evidences of increased survival of T cells. sγc was highly expressed in SF of RA patients and increased in established CIA mice. The therapeutic effect of PEG-aptamer was tested in CIA model and its treatment alleviated arthritis pathogenesis with impaired differentiation of pathogenic Th17, NKT1, and NKT17 cells in inflamed joint. Homodimeric sγc has pathogenic roles to exacerbate RA progression with differentiation of local Th17, NKT1, and NKT17 cells. Therefore, sγc is suggested as target of a therapeutic strategy for RA.

Indexed as

AgedAnimalsAptamers, NucleotideArthritis, ExperimentalArthritis, RheumatoidCell DifferentiationChitinase-3-Like Protein 1DimerizationFemaleHEK293 CellsHumansInflammationInterleukin-15Interleukin-2Interleukin Receptor Common gamma SubunitMiceAptamers, NucleotideCHI3L1 protein, humanChitinase-3-Like Protein 1IL15 protein, humanIL2 protein, humanIL2RG protein, humanIl2rg protein, mouseInterleukin-15Interleukin-2Interleukin Receptor Common gamma Subunitaptamercollagen-induced arthritisIL-2soluble common gamma chainTh17

Identifiers

PMID30800133
PMCPMC6375885
OpenAlexW2911315330

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.