Evidence map›Paper›PMID 30304822›Full record

ReviewCells2018

Pathogenic Role of Immune Cells in Rheumatoid Arthritis: Implications in Clinical Treatment and Biomarker Development.

Hooi-Yeen Yap, Sabrina Zi-Yi Tee, Magdelyn Mei-Theng Wong, Sook-Khuan Chow, Suat-Cheng Peh, Sin-Yeang Teow

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05422313 (Assessment of Galectin-9 in Rheumatoid Arthritis and Its Correlation With Disease Activity), which is not on this map. Cited by 209 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
209citing papers in PubMed, 5 pooled it
27.1field-weighted citation impact, top 1% 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.

NCT05422313 unknown statusnot on this mapstarted 2022, after this paper: background citation

Assessment of Galectin-9 in Rheumatoid Arthritis and Its Correlation With Disease Activity

TypeobservationalSponsorAssiut UniversityRan2022 to 2023Enrolled86ConditionsRheumatoid Arthritis
3 · Its place in the literature

Who cites it

209 citing papers in PubMed, 5 syntheses or guidelines pooled it, 471 citations in OpenAlex.

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  20. FOXC1-ATP7A Axis Activates PI3K/AKT Signaling to Suppress Cuproptosis and Drive Fibroblast Pathogenesis in Rheumatoid Arthritis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article

149 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

6 authors at 1 institution in 1 country.

Hooi-Yeen YapDepartment of Medical Sciences, School of Healthcare and Medical Sciences, Sunway University, Jalan Universiti, Bandar Sunway, 47500 Subang Jaya, Selangor Darul Ehsan, Malaysia. 17084351@imail.sunway.edu.my.
Sabrina Zi-Yi TeeDepartment of Medical Sciences, School of Healthcare and Medical Sciences, Sunway University, Jalan Universiti, Bandar Sunway, 47500 Subang Jaya, Selangor Darul Ehsan, Malaysia. sabrinateeziyi@yahoo.com.
Magdelyn Mei-Theng WongDepartment of Medical Sciences, School of Healthcare and Medical Sciences, Sunway University, Jalan Universiti, Bandar Sunway, 47500 Subang Jaya, Selangor Darul Ehsan, Malaysia. magdelyn.w@gmail.com.
Sook-Khuan ChowDepartment of Medical Sciences, School of Healthcare and Medical Sciences, Sunway University, Jalan Universiti, Bandar Sunway, 47500 Subang Jaya, Selangor Darul Ehsan, Malaysia. skhuanchow@gmail.com.
Suat-Cheng PehDepartment of Medical Sciences, School of Healthcare and Medical Sciences, Sunway University, Jalan Universiti, Bandar Sunway, 47500 Subang Jaya, Selangor Darul Ehsan, Malaysia. pehsc@sunway.edu.my.
Sin-Yeang TeowDepartment of Medical Sciences, School of Healthcare and Medical Sciences, Sunway University, Jalan Universiti, Bandar Sunway, 47500 Subang Jaya, Selangor Darul Ehsan, Malaysia. ronaldt@sunway.edu.my.ORCID 0000-0002-3824-0224
Sunway University · MY

Funding

National Cancer Council Malaysia MAKNA Grant 2016 EXT-SIDS-SIHD-MAKNA-2017-01Sunway Medical Centre Research Fund 2018 SRC/002/2017/FRSunway Medical Centre Research Fund 2018 SRC/003/2017/FRSunway University Internal Grant 2018 INT-2018-SHMS-SIHD-01
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a chronic, autoimmune, systemic, inflammatory disorder that affects synovial joints, both small and large joints, in a symmetric pattern. This disorder usually does not directly cause death but significantly reduces the quality of life and life expectancy of patients if left untreated. There is no cure for RA but, patients are usually on long-term disease modifying anti-rheumatic drugs (DMARDs) to suppress the joint inflammation, to minimize joint damage, to preserve joint function, and to keep the disease in remission. RA is strongly associated with various immune cells and each of the cell type contributes differently to the disease pathogenesis. Several types of immunomodulatory molecules mainly cytokines secreted from immune cells mediate pathogenesis of RA, hence complicating the disease treatment and management. There are various treatments for RA depending on the severity of the disease and more importantly, the patient's response towards the given drugs. Early diagnosis of RA and treatment with (DMARDs) are known to significantly improve the treatment outcome of patients. Sensitive biomarkers are crucial in early detection of disease as well as to monitor the disease activity and progress. This review aims to discuss the pathogenic role of various immune cells and immunological molecules in RA. This review also highlights the importance of understanding the immune cells in treating RA and in exploring novel biomarkers.

Indexed as

B-cellsbiomarkerDMARDsimmune cellsrheumatoid arthritisT-cellstreatment

Identifiers

PMID30304822
PMCPMC6211121
OpenAlexW2896285785

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.