Evidence map›Paper›PMID 41908154›Full record

ReviewJournal of pharmaceutical analysis2026

Promising TNF-α inhibitors: Targeting pathogenic TNF-α/TNFR signaling to restore Th17/Treg balance in rheumatoid arthritis.

Jiajie Kuai, Zhuo Chen, Ju He, Fengling Wang, Wei Wei

Abstract readReview
In one paragraph

Review in Journal of pharmaceutical analysis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  3. Article
  4. Review
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

5 authors.

Jiajie KuaiInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immune Medicine (Anhui Medical University), Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei, 230032, China.
Zhuo ChenInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immune Medicine (Anhui Medical University), Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei, 230032, China.
Ju HeInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immune Medicine (Anhui Medical University), Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei, 230032, China.
Fengling WangInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immune Medicine (Anhui Medical University), Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei, 230032, China.
Wei WeiInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immune Medicine (Anhui Medical University), Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei, 230032, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pleiotropic regulatory effect of tumor necrosis factor-alpha (TNF-α), an essential cytokine involved in immune regulation, is of significant importance in the immune response. TNF-α inhibitors have been widely used in rheumatoid arthritis (RA) and other autoimmune diseases since their introduction into clinical practice. However, the tradeoff between its excellent efficacy and adverse drug reactions (ADR) remains a problem. T cells, especially the T helper cell 17 (Th17)/regulatory T (Treg) cells balance, are crucial for the treatment of autoimmune diseases including RA. This review explores the mechanisms by which TNF-α/TNF receptor (TNFR) signaling induces Th17/Treg imbalance in RA. This review synthesizes current knowledge to facilitate an improved understanding of the causes of ADR, such as infection caused by TNF-α inhibitors in clinical practice. Moreover, our findings offer a reference for exploring potential TNF-α/TNFR signaling inhibitory strategies from the perspective of regulating T cell balance.

Indexed as

Rheumatoid arthritisTh17TNFRTNF-αTNF-α inhibitorsTreg

Identifiers

PMID41908154
PMCPMC13018864

What OpenQuestion holds

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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.