ReviewMedicine2026
IL-33-induced neuroimmune regulation in depression: A narrative review from molecular mechanisms to therapeutic potential.
Review in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Engineering Advanced Nanomedicine Against Depression: From Treatment Challenges to Delivery Strategies.Advanced healthcare materials · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depression is a common mental illness characterized by significant variability in treatment response and resistance to current antidepressant drugs and psychotherapy. Recent advances in neuroimmunology have highlighted the immune system's crucial role in the pathogenesis of depression. This review explores the dual roles of interleukin-33 (IL-33) in neuroimmune regulation, neuroinflammation, and neuroplasticity, aiming to investigate its potential as a therapeutic target for depression. An integrative review of the literature was conducted, focusing on the molecular mechanisms of IL-33 in neuroinflammation and its impact on microglia, astrocytes, and the hypothalamic-pituitary-adrenal axis. Animal model studies and clinical evidence regarding IL-33 levels in depression were also analyzed. IL-33 exhibits both pro-inflammatory and anti-inflammatory functions and regulates key immune cells in the central nervous system, including microglia and astrocytes. It regulates neuroinflammation and improves neural plasticity, which is often impaired in depression. Clinical studies show decreased IL-33 levels in the blood and cerebrospinal fluid of depression patients, correlating with disease severity. IL-33 holds promise as a potential biomarker for depression and may serve as a therapeutic target. Recent therapeutic strategies targeting its receptor (suppression of tumorigenicity 2) and signaling pathways are under investigation, with early clinical trials focusing on anti-IL-33 receptor antibodies and signaling pathway inhibitors. However, challenges remain regarding immune-related side effects, and further clinical studies are needed to ensure the safety and efficacy of IL-33-targeted therapies.
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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 Socratic graph.