ReviewFrontiers in immunology2025
Mini review: Interleukin-32 as a key mediator of type 1 diabetes pathogenesis.
Review in Frontiers in immunology, 2025. 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
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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.
- The Framework of Host Innate and Adaptive Immunological Pathways.Biomedicines · 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing β-cells in the pancreatic islets. The pathogenesis, involving complex interactions between genetic susceptibility and environmental factors, is mediated by T cells driven by multiple stimuli including cytokines. Interleukin-32 (IL-32), a predominantly proinflammatory cytokine, has emerged as a potential contributor to T1D pathogenesis. In this review we discuss current knowledge of IL-32 and its role in T1D pathogenesis, examining expression patterns in PBMCs and islets, possible functional mechanisms, and the potential for IL-32 as a biomarker. We will also consider how immunotherapies currently in clinical trials aiming to slow T1D progression may impact IL-32.
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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 OpenQuestion graph.