Volume 83, Issue 10 (January 2025)
Tehran Univ Med J. 2025, 83(10): 698-704 |
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Kaveh A, Amiri B, Kiaee F, Shahi H. beta cells, diabetes, interleukin 32, type 1 diabetes.. Tehran Univ Med J. 2025; 83 (10) :698-704
URL: http://tumj.tums.ac.ir/article-1-13880-en.html
URL: http://tumj.tums.ac.ir/article-1-13880-en.html
1- Department of Pediatrics, Akbar Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
2- Department of Pediatric Diseases, Mashhad Medical Sciences Campus, Islamic Azad University, Mashhad, Iran.
3- Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran.
4- Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. ,Shahi@sbmu.ac.ir
2- Department of Pediatric Diseases, Mashhad Medical Sciences Campus, Islamic Azad University, Mashhad, Iran.
3- Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran.
4- Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. ,
Abstract: (49 Views)
Autoimmune destruction of insulin-producing beta cells in the islets of Langerhans of the pancreas by specific T cells causes type 1 diabetes mellitus. Among the various inflammatory factors involved in type 1 diabetes, cytokines play a critical role in coordinating immune responses and cell destruction. Until recently, relatively little information was available about IL-32. This article reviews the role of interleukin 32 in the human immune system and its effects on the development of type 1 diabetes. To search and select English-language articles in PubMed, the MESH format with the keywords "interleukin 32" and "diabetes mellitus, type 1" was used for this review. The original articles referenced in this review were published between 2005 and 2025. Articles that were in the form of letters to the editor, reviews, or case reports were not included in this study. The complex effects of interleukin-32 in the pathogenesis of type 1 diabetes is supported by growing evidence that refer to its dysregulated expression and potent pro-inflammatory rolls. Elevated levels of IL-32, which includes its various splice variants (isoforms), are observed in various inflammatory and autoimmune studies and diseases, including type 1 diabetes. Specifically, studies have shown significantly increased IL-32 expression in peripheral blood mononuclear cells (PBMCs) of T1D patients compared to healthy control group. High levels of IL-32 in peripheral blood immune cells and hypomethylation of the IL32 promoter in CD8+ T cells of T1D patients suggest its role in the pathology of this disease. IL-32, It was shown that to interact with proteinase 3 (PR3), thereby facilitating the processing and activation of pro-IL-1β and pro-IL-18 into their functional and biological active form. IL-32 often has pro-inflammatory actions and induces cytokines such as TNFα and IL-6. There is a growing body of evidence that places IL-32 as a key cytokine involved in the pathogenesis of autoimmune type 1 diabetes. However, the expression and functions of different isoforms, especially IL-32β, which may have anti-inflammatory actions, remain to be elucidated.
Type of Study: Review Article |
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