预防和治疗 1 型糖尿病:寻找针对多种免疫代谢途径的理想联合疗法

M. Pinheiro, Felipe Moura Maia Pinheiro, M. Garo, D. Pastore, F. Pacifici, Camillo Ricordi, D. Della-Morte, Marco Infante
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摘要

1 型糖尿病(T1D)是一种自身免疫性疾病,是由于胰腺朗格汉斯胰岛中产生胰岛素的 beta 细胞在免疫介导下逐渐遭到破坏,导致终生需要外源性胰岛素治疗。据最新估计,目前全球约有 840 万人患有 T1D。由于目前还没有彻底治愈这种疾病的生物方法,因此亟需新型治疗策略,以安全有效地改变该疾病在各个阶段的自然病史。治疗 T1D 的理想目标包括预防自身免疫性 beta 细胞破坏、保留残余 beta 细胞数量和内源性胰岛素分泌、替换和/或再生 beta 细胞,以及通过先进的闭环人工胰腺系统自动输送胰岛素。在这方面,一个重要的研究领域是研究免疫治疗和β细胞保护剂,将其作为改变疾病的疗法,以防止或消除胰岛素依赖性,从而找到彻底治愈 T1D 的生物方法。在这篇评论中,我们将讨论为什么针对与 T1D 相关的多种免疫代谢功能障碍(β 细胞自身免疫除外)使用联合疗法可能比使用单一疗法更能有效地保护处于 T1D 不同阶段的个体的 β 细胞功能。
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Prevention and treatment of type 1 diabetes: in search of the ideal combination therapy targeting multiple immunometabolic pathways
Type 1 diabetes (T1D) represents an autoimmune disease caused by the gradual immune-mediated destruction of the insulin-producing beta cells within the pancreatic islets of Langerhans, resulting in the lifelong need for exogenous insulin therapy. According to recent estimates, T1D currently affects about 8.4 million individuals worldwide. Since a definitive biological cure for this disease is not available yet, there is a great need for novel therapeutic strategies aimed at safely and effectively altering the natural history of the disease during its sequential stages. Ideal therapeutic goals in T1D include the prevention of autoimmune beta-cell destruction, the preservation of residual beta-cell mass and endogenous insulin secretion, the replacement and/or regeneration of beta cells, as well as automated insulin delivery through advanced closed-loop artificial pancreas systems. With this regard, an important research area focused on the identification of a definitive biological cure for T1D is represented by the investigation of immunotherapeutic and beta-cell-protective agents used as disease-modifying therapies to forestall or eliminate insulin dependence. In this commentary, we discuss the reasons why the use of combination therapies targeting the multiple immunometabolic dysfunctions associated with T1D (other than beta-cell autoimmunity) is likely to be more effective in preserving beta cell function in individuals at different stages of T1D, as compared to the use of single therapeutic agents.
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