糖尿病是全球增长最快的慢性疾病，患病率增长速度超过心脏病和癌症。虽然该疾病在临床上表现为慢性高血糖状态，但已经识别出两种不同亚型。1型糖尿病（T1D）被描述为一种自身免疫性疾病，其中胰岛素产生的胰岛β细胞受到破坏，而2型糖尿病（T2D）则是由代谢不足引起的，其中胰岛素产生不足和/或胰岛素作用减弱。目前明显的是，促炎反应导致功能性β细胞数量的减少，这是T1D和T2D的共同的潜在机制。巨噬细胞是两种疾病发病机制中的中心免疫细胞，对于引起炎症反应和损害β细胞功能的初始和持续起着重要的作用。此外，巨噬细胞与β细胞之间的相互作用协调了炎症反应和随之而来的β细胞功能和破坏。相反，这种相互作用可以引起免疫耐受和保护β细胞数量和功能。因此，专门针对巨噬细胞和β细胞之间的细胞间通讯提供了一种防止/停止T1D和T2D潜在胰岛炎症事件的独特策略。由于寄生虫（蠕虫）及其排泄/分泌物具有调节哺乳动物免疫反应的强效能力，因此已经研究其作为T1D和T2D的治疗剂的潜力。此项研究在临床和动物模型中取得了积极的预防疾病的结果。然而，研究的重点是在免疫细胞及其效应物的调节上，忽略了蠕虫及其产物对β细胞的直接影响以及对巨噬细胞和β细胞之间信号交流的调节。本综述探讨了蠕虫及其产物引发的巨噬细胞改变如何影响与β细胞的相互作用，促进其功能和存活。此外，讨论了寄生虫来源产物与内分泌细胞的直接作用，以影响其与巨噬细胞的通讯，以预防β细胞死亡并增强功能。内分泌细胞与巨噬细胞之间双向代谢对话的新模式为治疗免疫介导的代谢疾病开辟了新的途径。Copyright © 2023 Camaya, O’Brien and Donnelly.

Diabetes is the fastest growing chronic disease globally, with prevalence increasing at a faster rate than heart disease and cancer. While the disease presents clinically as chronic hyperglycaemia, two distinct subtypes have been recognised. Type 1 diabetes (T1D) is characterised as an autoimmune disease in which the insulin-producing pancreatic β-cells are destroyed, and type 2 diabetes (T2D) arises due to metabolic insufficiency, in which inadequate amounts of insulin are produced, and/or the actions of insulin are diminished. It is now apparent that pro-inflammatory responses cause a loss of functional β-cell mass, and this is the common underlying mechanism of both T1D and T2D. Macrophages are the central immune cells in the pathogenesis of both diseases and play a major role in the initiation and perpetuation of the proinflammatory responses that compromise β-cell function. Furthermore, it is the crosstalk between macrophages and β-cells that orchestrates the inflammatory response and ensuing β-cell dysfunction/destruction. Conversely, this crosstalk can induce immune tolerance and preservation of β-cell mass and function. Thus, specifically targeting the intercellular communication between macrophages and β-cells offers a unique strategy to prevent/halt the islet inflammatory events underpinning T1D and T2D. Due to their potent ability to regulate mammalian immune responses, parasitic worms (helminths), and their excretory/secretory products, have been examined for their potential as therapeutic agents for both T1D and T2D. This research has yielded positive results in disease prevention, both clinically and in animal models. However, the focus of research has been on the modulation of immune cells and their effectors. This approach has ignored the direct effects of helminths and their products on β-cells, and the modulation of signal exchange between macrophages and β-cells. This review explores how the alterations to macrophages induced by helminths, and their products, influence the crosstalk with β-cells to promote their function and survival. In addition, the evidence that parasite-derived products interact directly with endocrine cells to influence their communication with macrophages to prevent β-cell death and enhance function is discussed. This new paradigm of two-way metabolic conversations between endocrine cells and macrophages opens new avenues for the treatment of immune-mediated metabolic disease.Copyright © 2023 Camaya, O’Brien and Donnelly.