MINI REVIEW article
Front. Immunol.
Sec. Cytokines and Soluble Mediators in Immunity
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1641698
This article is part of the Research TopicThe Biological / Pathological Role of IL-32 in Health / DiseaseView all 6 articles
Mini Review: Interleukin-32 as a key mediator of type 1 diabetes pathogenesis
Provisionally accepted
- Cardiff University Cardiff Division of Infection and Immunity, Cardiff, United Kingdom
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Type 1 diabetes (T1D) is an autoimmune disease characterised 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.
Keywords: IL-32, type 1 diabetes, Immunotherapy, T cells, beta cells, β-cells
Received: 05 Jun 2025; Accepted: 11 Aug 2025.
Copyright: © 2025 Pearson and Hanna. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Stephanie J Hanna, Cardiff University Cardiff Division of Infection and Immunity, Cardiff, United Kingdom
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