Evidence map›Paper›PMID 40580299›Full record

ReviewInflammopharmacology2025

Targeting the double-edged sword: cytokines in the pathogenesis and treatment of autoimmune diseases.

Fatima Dandash, Zahraa Salhab, Rawan Issa, Zeinab Al Dirani, Mariam Hamze, Gabriel Fares, Fatima Berro, Fatima Shaalan, Ali Hamade, Makram Merimi and 5 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
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.

Fatima Dandash *Laboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon.
Zahraa Salhab *Laboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon.
Rawan IssaLaboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon.
Zeinab Al DiraniLaboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon.
Mariam HamzeLaboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon.
Gabriel FaresLaboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon.
Fatima BerroLaboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon.
Fatima ShaalanLaboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon.
Ali HamadeSchool of Arts and Sciences, Lebanese American University, Beirut, Lebanon.
Makram MerimiLBBES Laboratory, Genetics and Immune Cell Therapy Unit, Faculty of Sciences, University Mohammed Premier, 60000, Oujda, Morocco.
Mehdi NajarFaculty of Medicine, Université Libre de Bruxelles, ULB721, 1070, Brussels, Belgium.
Rayan DakroubLaboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon.
Douaa KhreisLaboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon.
Mohammad Fayyad-Kazan *College of Arts and Sciences, Department of Natural and Applied Sciences, The American University of Iraq-Baghdad (AUIB), 10001, Baghdad, Iraq. mfayyadk@gmail.com.ORCID http://orcid.org/0000-0001-8442-1619
Hussein Fayyad-KazanLaboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon. hfayyadk@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune diseases are often idiopathic, with complex immune cell interactions that remain poorly understood. Cytokines, signaling molecules with a dual nature, play a pivotal role in these conditions. While they are essential for regulating immune responses and have therapeutic applications, they can also contribute to inflammation and the development of autoimmune disorders. Key cytokines such as tumor necrosis factor -α (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-17 (IL-17), interleukin-23 (IL-23), granulocyte-macrophage colony-stimulating factor (GM-CSF), and interferon-gamma (IFN-γ) have been implicated in the pathogenesis of autoimmune diseases like inflammatory bowel disease (IBD), multiple sclerosis (MS), and rheumatoid arthritis (RA). This review aims to explore the dual role of cytokines in autoimmune diseases, focusing on their involvement in disease pathogenesis and their potential as therapeutic targets. It evaluates the mechanisms and clinical outcomes of anti-cytokine inhibitors while highlighting gaps in current research that could pave the way for improved treatments. Anti-cytokine therapies have shown significant promise in managing conditions like IBD, MS, and RA, but challenges remain in optimizing their efficacy and minimizing side effects. Further research is needed to better understand the intricate roles of cytokines in autoimmunity and to refine therapeutic strategies, ultimately improving patient outcomes.

Indexed as

Autoimmune DiseasesCytokinesAnimalsHumansInflammationCytokinesAnti-cytokine therapiesAutoimmune diseasesCytokinesInflammation

Identifiers

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.