Treg in type 1 diabetes
Treg in type 1 diabetes
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DOI：
10.1007/s12013-007-0018-5
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发表时间：
2007-01-01
影响因子：
2.6
通讯作者：
Atkinson, Mark
中科院分区：
文献类型：
--
作者：
Brusko, Todd;Atkinson, Mark
在撰写本文时，存在一个主要的空白;缺乏预防和/或逆转人类1型糖尿病的方法。我们认为这种空白在很大程度上是由于我们缺乏对自身免疫机制的理解，这些机制是β细胞破坏的基础，未能理解导致1型糖尿病的免疫因素，以及缺乏免疫学工具，这些工具可以更好地理解疾病发展和监测治疗干预的机制。因此，最近产生了强烈的研究兴趣，以了解调节免疫应答并形成免疫耐受状态的机制。虽然已经朝着这些目标取得了一些进展，但还需要进行更多的研究来解决上述知识空白，包括调节性T细胞（Treg）在1型糖尿病发病机制和自然史中的作用，该作用由其CD 4和CD 25以及转录因子FOXP 3的共表达来定义。我们和其他人最近报道了与Treg细胞在1型糖尿病中的频率和功能相关的发现，但由此产生的文献代表了一些相互矛盾的发现。我们的研究不支持改变的Treg频率与1型糖尿病相关的观点，而是确定了功能性（即，抑制）这些细胞在患有疾病的受试者中的活性。需要解决上述已发表的Treg在1型糖尿病中的频率和功能差异，这是这项重要综述的动力。此外，我们希望强调扩大研究的必要性，以解决与Treg频率和功能相关的细胞和分子机制的具体知识差距。
At the time of this writing, a major void exists; the lack of a method to prevent and/or reverse type 1 diabetes in humans. We believe this void to a large extent is the result of our lack in understanding the mechanisms of autoimmunity that underlie beta cell destruction, a failure to understand the immunologic factors that contribute to type 1 diabetes, and the absence of immunologic tools which would allow for a better understanding of the mechanisms underlying disease development and monitoring of therapeutic interventions. Due to this, an intense degree of research interest has recently been generated to understand the mechanisms that regulate the immune response and form a state of immunological tolerance. While some progress has been made towards these goals, additional investigations are needed to address the aforementioned knowledge voids including the role for regulatory T cells (Treg), defined by their co-expression of CD4 and CD25 as well as the transcription factor FOXP3, in the pathogenesis and natural history of type 1 diabetes. We and others have recently reported findings related to the frequency and function of Treg cells in type 1 diabetes, yet the resulting literature represents a somewhat conflicting body of findings. Our studies did not support the notion that altered Treg frequencies are associated with type 1 diabetes, but rather did identify alterations in the functional (i.e., suppressive) activities of these cells in subjects with the disease. The need to bring resolution to the aforementioned published discrepancies in frequency and function of Treg in type 1 diabetes represents the impetus for this critical review. In addition, we hope to highlight the need for expanded studies that address specific knowledge gaps regarding the cellular and molecular mechanism(s) related to the frequency and function of Treg.