Barbara Davis Center for Diabetes, University of Colorado, Aurora, CO 80045, USA.
Int J Mol Sci. 2022 Mar 15;23(6):3155. doi: 10.3390/ijms23063155.
While progress has been made toward understanding mechanisms that lead to the development of autoimmunity, there is less knowledge regarding protective mechanisms from developing such diseases. For example, in type 1 diabetes (T1D), the immune-mediated form of diabetes, the role of pathogenic T cells in the destruction of pancreatic islets is well characterized, but immune-mediated mechanisms that contribute to T1D protection have not been fully elucidated. One potential protective mechanism includes the suppression of immune responses by regulatory CD4 T cells (Tregs) that recognize self-peptides from islets presented by human leukocyte antigen (HLA) class II molecules. In this review, we summarize what is known about the antigenic self-peptides recognized by Tregs in the context of T1D.
虽然在理解导致自身免疫发展的机制方面已经取得了进展，但对于预防此类疾病的保护机制的了解较少。例如，在 1 型糖尿病 (T1D) 中，这种免疫介导的糖尿病形式，致病性 T 细胞在破坏胰岛方面的作用已得到很好的描述，但有助于 T1D 保护的免疫介导机制尚未完全阐明。一种潜在的保护机制包括由识别胰岛自身肽的调节性 CD4 T 细胞 (Tregs) 抑制免疫反应，这些自身肽由人类白细胞抗原 (HLA) 类 II 分子呈递。在这篇综述中，我们总结了已知的在 T1D 背景下 Tregs 识别的抗原自身肽。
