Evidence map›Paper›PMID 41532007›Full record

ReviewMediators of inflammation2026

Decoy Receptors in Autoimmunity: Molecular Guardians and Pathogenic Players in Immune Dysregulation.

Hadiseh Farahani, Parviz Kokhaei, Ali Ganji, Ghasem Mosayebi, Ali Ghazavi

Abstract readReview
In one paragraph

Review in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. 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.

Hadiseh FarahaniDepartment of Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran, arakmu.ac.ir.
Parviz KokhaeiDepartment of Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran, arakmu.ac.ir.
Ali GanjiDepartment of Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran, arakmu.ac.ir.
Ghasem MosayebiDepartment of Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran, arakmu.ac.ir.
Ali GhazaviDepartment of Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran, arakmu.ac.ir.ORCID https://orcid.org/0000-0002-4219-9594

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune disorders encompass a varied range of diseases in which the immune system mistakenly targets and attacks the body's own tissues. The causes of the conditions are unknown. It is presumed that various genetic, environmental, and immune factors all play a part. Nowadays, therapies concentrate mainly on anti-inflammatory agents with immunosuppressant medications. New research highlights the central role of decoy receptors (DcRs) in regulating the immune system. DcRs are molecular traps for cytokines and other signaling molecules, preventing them from binding to functional receptors and influencing inflammatory processes. Their activity is context-dependent, shifting the balance between protective and pathogenic responses, and DcR dysregulation has been implicated in the development of autoimmune diseases. Understanding DcR function is critical for the design of potential therapeutic interventions. DcR mechanisms are reviewed here with emphasis on structural and disease-specific functions. Targeting DcRs is a promising strategy to reconstitute immune homeostasis. Understanding the dual regulatory functions and context-dependent mechanisms is critical for designing new therapies that reduce autoimmune pathogenesis without compromising host defense mechanisms.

Indexed as

AutoimmunityAnimalsAutoimmune DiseasesCytokinesHumansImmune SystemInflammationSignal TransductionCytokinesautoimmune diseasedecoy receptorimmune regulationinflammation

Identifiers

PMID41532007
PMCPMC12791581

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.