Recent reports have revived interest in the active role that β-cells may play in type 1 diabetes pathogenesis at different stages of disease. In some studies, investigators suggested an initiating role and proposed that type 1 diabetes may be primarily a disease of β-cells and only secondarily a disease of autoimmunity. This scenario is possible and invites the search for environmental triggers damaging β-cells. Another major contribution of β-cells may be to amplify autoimmune vulnerability and to eventually drive it into an intrinsic, self-detrimental state that turns the T cell–mediated homicide into a β-cell suicide. On the other hand, protective mechanisms are also mounted by β-cells and may provide novel therapeutic targets to combine immunomodulatory and β-cell protective agents. This integrated view of autoimmunity as a disease of T-cell/β-cell cross talk will ultimately advance our understanding of type 1 diabetes pathogenesis and improve our chances of preventing or reversing disease progression.

中文翻译：

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1 型糖尿病发病机制中的 β 细胞：环境的受害者还是悲剧事件的煽动者？

最近的报告重新引起了人们对 β 细胞在 1 型糖尿病不同阶段发病机制中可能发挥的积极作用的兴趣。在一些研究中，研究人员提出了一种始动作用，并提出 1 型糖尿病可能主要是一种 β 细胞疾病，其次是一种自身免疫性疾病。这种情况是可能的，并需要寻找破坏 β 细胞的环境触发因素。β细胞的另一个主要贡献可能是放大自身免疫的脆弱性，并最终使其进入一种内在的、自我伤害的状态，将T细胞介导的杀人转变为β细胞自杀。另一方面，β细胞也具有保护机制，并可能为结合免疫调节剂和β细胞保护剂提供新的治疗靶点。这种将自身免疫视为 T 细胞/β 细胞串扰疾病的综合观点将最终促进我们对 1 型糖尿病发病机制的理解，并提高我们预防或逆转疾病进展的机会。