Asif Roha, Khalid Ammara, Mercantepe Tolga, Klisic Aleksandra, Rafaqat Sana, Rafaqat Saira, Mercantepe Filiz
Department of Biotechnology, Lahore College for Women University, Lahore 44444, Pakistan.
Department of Histology, Faculty of Medicine, Recep Tayyip Erdogan University, Rize 53100, Türkiye.
Diagnostics (Basel). 2025 Jul 30;15(15):1906. doi: 10.3390/diagnostics15151906.
: Despite distinct etiologies, type 1 diabetes (T1D) and type 2 diabetes (T2D) share chronic inflammation as a core feature. Interleukins, key immune mediators, play important yet still not fully understood roles in the development and complications of both conditions. : This narrative review aims to provide a comprehensive and critical synthesis of current evidence on the role of key interleukins in T1D and T2D, highlighting their immunological functions, genetic associations, clinical correlations, and translational potential. : A targeted literature search was conducted in PubMed, Google Scholar, and ScienceDirect up to January 2025, focusing on English-language clinical and experimental studies involving interleukins and their relevance to T1D and T2D. Reference lists were manually screened for additional sources. Interleukins (ILs) were reviewed individually to assess their immunobiology, disease specificity, and biomarker or therapeutic value. : Pro-inflammatory cytokines such as IL-1β, IL-6, and IL-17 contribute to islet inflammation, insulin resistance, and microvascular damage in both T1D and T2D. Anti-inflammatory mediators including IL-4, IL-10, and IL-13 exhibit protective effects but vary in expression across disease stages. Less-characterized interleukins such as IL-3, IL-5, IL-9, and IL-27 demonstrate dual or context-dependent roles, particularly in shaping immune tolerance and tissue-specific complications such as nephropathy and neuropathy. Polymorphisms in IL-10 and IL-6 genes further suggest genetic contributions to interleukin dysregulation and metabolic dysfunction. Despite promising insights, translational gaps persist due to overreliance on preclinical models and limited longitudinal clinical data. : Interleukins represent a mechanistic bridge linking immune dysregulation to metabolic derangements in both T1D and T2D. While their diagnostic and therapeutic potential is increasingly recognized, future research must address current limitations through isoform-specific targeting, context-aware interventions, and validation in large-scale, human cohorts. A unified interleukin-based framework may ultimately advance personalized strategies for diabetes prevention and treatment.
尽管1型糖尿病（T1D）和2型糖尿病（T2D）病因不同，但慢性炎症是它们的共同核心特征。白细胞介素作为关键的免疫介质，在这两种疾病的发生发展及并发症中发挥着重要作用，但其作用机制仍未完全明确。 本叙述性综述旨在全面、批判性地综合当前关于关键白细胞介素在T1D和T2D中作用的证据，重点阐述其免疫功能、基因关联、临床相关性及转化潜力。 截至2025年1月，在PubMed、谷歌学术和ScienceDirect上进行了有针对性的文献检索，重点关注涉及白细胞介素及其与T1D和T2D相关性的英文临床和实验研究。手动筛选参考文献列表以获取更多来源。对白细胞介素（ILs）进行单独综述，以评估其免疫生物学、疾病特异性以及生物标志物或治疗价值。 促炎细胞因子如IL-1β、IL-6和IL-17在T1D和T2D中均导致胰岛炎症、胰岛素抵抗和微血管损伤。抗炎介质包括IL-4、IL-10和IL-13具有保护作用，但在疾病各阶段的表达有所不同。特征尚不明确的白细胞介素如IL-3、IL-5、IL-9和IL-27表现出双重或依赖于背景的作用，尤其是在塑造免疫耐受和组织特异性并发症（如肾病和神经病变）方面。IL-10和IL-6基因的多态性进一步表明基因对白细胞介素失调和代谢功能障碍有影响。尽管有一些有前景的见解，但由于过度依赖临床前模型和有限的纵向临床数据，转化差距仍然存在。 白细胞介素是连接T1D和T2D中免疫失调与代谢紊乱的机制桥梁。虽然它们的诊断和治疗潜力越来越受到认可，但未来的研究必须通过亚型特异性靶向、情境感知干预以及在大规模人类队列中的验证来解决当前的局限性。基于白细胞介素的统一框架最终可能推动糖尿病预防和治疗的个性化策略。
