Letter to the Editor
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Oct 15, 2024; 15(10): 2147-2151
Published online Oct 15, 2024. doi: 10.4239/wjd.v15.i10.2147
Interleukin-35: A key player managing pre-diabetes and chronic inflammatory type 1 autoimmune diabetes
Ratul Chakraborty, Ashis Kumar Mukherjee, Asis Bala
Ratul Chakraborty, Ashis Kumar Mukherjee, Life Sciences Division, Institute of Advanced Study in Science and Technology, Guwahati 781035, Guwahati, Assam, India
Asis Bala, Pharmacology and Drug Discovery Research Laboratory, Division of Life Sciences, Institute of Advanced Study in Science and Technology, Guwahati 781035, Assam, India
Author contributions: Bala A was responsible for planning and writing; Chakraborty R systematically formatted the manuscript; Mukherjee AK revised the manuscript with data analysis.
Conflict-of-interest statement: All of the authors have no relevant financial or non-financial interests to disclose.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Asis Bala, PhD, Associate Professor, Pharmacology and Drug Discovery Research Laboratory, Division of Life Sciences, Institute of Advanced Study in Science and Technology, Vigyan Path, Guwahati 781035, Assam, India. asisbala@iasst.gov.in
Received: March 25, 2024
Revised: August 16, 2024
Accepted: August 26, 2024
Published online: October 15, 2024
Processing time: 185 Days and 3.5 Hours
Abstract

Interleukin-35 (IL-35) is a novel protein comprising IL-12α and IL-27β chains. The IL12A and EBI3 genes are responsible for its production. The study of IL-35 has experienced a substantial increase in interest in recent years, as demonstrated by many research papers. Recent clinical studies have shown that individuals who do not have a C-peptide have notably reduced amounts of IL-35 in their blood serum. This is accompanied by a drop in the percentage of IL-35+ Treg cells, regulatory B cells, and CD8+ FOXP3+ cells that produce IL-35. This article em-phasizes the potential significance of IL-35 expression in governing the immune response and its involvement in chronic inflammatory autoimmune diabetes in pancreatic inflammation. It demonstrates IL-35's ability to regulate cytokine proportions, modulate B cells, and protect against autoimmune diabetes. However, further investigation is necessary to ascertain the precise mechanism of IL-35, and meticulous planning is essential for clinical studies.

Keywords: Interleukin-35; Chronic inflammatory type diabetes; Autoimmune diabetes; Pancreatic inflammation; Gene disease association

Core Tip: Studies suggest interleukin (IL)-35 protects against prediabetes and autoimmune diabetes by regulating immune system function. Development of type 1 diabetes (T1D) can be influenced by various cytokines produced by immune and pancreatic cells. Some cytokines, such as IL-10, transforming growth factor beta (TGF-β), IL-5, IL-4, IL-2, IL-15, IL-33, and IL-35, can stimulate regulatory cells in the immune system, releasing anti-inflammatory cytokines. Regulatory dendritic cells release IL-7, important for maintaining Tregs. In T1D, Tregs express IL-7Rα. Inhibiting TGF-β and activating IFN-γ can increase TC, Th1, and Th17 cells, while TGF-β can stimulate Runx1 expression to convert Th1 cells into Th17 cells.