Evidence map›Paper›PMID 40355878›Full record

ReviewJournal of inflammation (London, England)2025

Biological mechanisms and therapeutic prospects of interleukin-33 in pathogenesis and treatment of allergic disease.

Mohammad Chand Jamali, Asma'a H Mohamed, Azfar Jamal, Mohammad Azhar Kamal, Waleed Al Abdulmonem, Bashar Abdullah Saeed, Nasrin Mansuri, Fuzail Ahmad, Mustafa Mudhafar, Alaa Shafie and 1 more

Abstract readReview
In one paragraph

Review in Journal of inflammation (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. CommensalFrontiers in immunology · 2025
    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

11 authors.

Mohammad Chand JamaliFaculty of Medical and Health Sciences, Liwa College, Al Ain, Abu Dhabi, UAE.
Asma'a H MohamedDepartment of Optometry Techniques, Technical College Al-Mussaib, Al-Furat Al-Awsat Technical University, Najaf, Iraq. asmaa.muhammed@atu.edu.iq.
Azfar JamalDepartment of Biology, College of Science, Al-Zulfi, Majmaah University, Al-Majmaah 11952,, Saudi Arabia.
Mohammad Azhar KamalDepartment of Pharmaceutics, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Alkharj 11942, Saudi Arabia.
Waleed Al AbdulmonemDepartment of Pathology, College of Medicine, Qassim University, Buraidah, Kingdom of Saudi Arabia.
Bashar Abdullah SaeedDepartment of Medical Laboratory Technics, Al-Noor University College, Nineveh, Iraq.
Nasrin MansuriClinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia.
Fuzail AhmadRespiratory Care Department, College of Applied Sciences, Almaarefa University, Diriya, Riyadh 13713 , Saudi Arabia.
Mustafa MudhafarDepartment of Medical Physics, Faculty of Medical Applied Sciences, University of Kerbala, 56001, Karbala, Iraq.
Alaa ShafieDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, P.O.Box 11099, Taif, 21944, Saudi Arabia.
Haroonrashid M HattiwaleDepartment of Basic Medical Sciences, College of Medicine, Majmaah University, Al-Majmaah 11952 , Saudi Arabia. h.hattiwale@mu.edu.sa.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allergic diseases significantly impact the quality of life of people around the world. Cytokines play a crucial role in regulating the immune system. Due to their importance in pro-inflammatory mechanisms, cytokines are used to understand pathogenesis and serve as biomarkers in many diseases. One such cytokine is interleukin-33, a member of the IL-1 family, including IL- 1α, IL-1β, and IL-18. The IL-33 receptor is a heterodimer of IL-1 receptor-like 1 and IL-1 receptor accessory protein. IL-33 plays a critical role in regulating innate and adaptive immune responses. The primary targets of IL-33 in vivo are tissue-resident immune cells, including mast cells, group 2 innate lymphoid cells, regulatory T cells, T helper 2 cells, eosinophils, basophils, dendritic cells, Th1 cells, CD8 + T cells, NK cells, iNKT cells, B cells, neutrophils, and macrophages. However, IL-33 appears to act as an alarm signal that is promptly released by producing cells under cellular damage or stress conditions. IL-33 regulates signaling and various biological functions, including induction of pro-inflammatory cytokines, regulation of cell proliferation, and involvement in tissue remodeling. IL-33 is fundamental in immune-related diseases and plays a critical role in the control of inflammation. Recently, IL-33 has been shown to significantly impact allergic diseases, primarily by inducing Th2 immune responses. IL-33 is a key regulator of mast cell function and a promising therapeutic target for treating allergic diseases. This review provides an overview of the current understanding of the role of IL-33 in allergy pathogenesis and potential clinical approaches.

Indexed as

Allergic diseasesIL-33 receptorImmune systemInterleukin-33MyD88

Identifiers

PMID40355878
PMCPMC12070619

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.