Pearson, James A. ![]() ![]() |
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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.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Schools > Medicine |
Publisher: | Frontiers Media |
ISSN: | 1664-3224 |
Date of First Compliant Deposit: | 5 September 2025 |
Date of Acceptance: | 11 August 2025 |
Last Modified: | 05 Sep 2025 15:00 |
URI: | https://orca.cardiff.ac.uk/id/eprint/180942 |
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