Department of Immunology and Microbiology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Department of Biomedical Research, National Jewish Health, Denver, CO, USA.
Clin Exp Immunol. 2019 Dec;198(3):314-325. doi: 10.1111/cei.13353. Epub 2019 Aug 30.
Inhibition of immune cell trafficking to the pancreatic islets during type 1 diabetes (T1D) has therapeutic potential, since targeting of T cell and B cell trafficking has been clinically effective in other autoimmune diseases. Trafficking to the islets is characterized by redundancy in adhesion molecule and chemokine usage, which has not enabled effective targeting to date. Additionally, cognate antigen is not consistently required for T cell entry into the islets throughout the progression of disease. However, myeloid cells are required to enable T cell and B cell entry into the islets, and may serve as a convergence point in the pathways controlling this process. In this review we describe current knowledge of the factors that mediate immune cell trafficking to pancreatic islets during T1D progression.
在 1 型糖尿病（T1D）期间抑制免疫细胞向胰岛的迁移具有治疗潜力，因为针对 T 细胞和 B 细胞迁移的靶向治疗在其他自身免疫性疾病中已被临床证明是有效的。向胰岛的迁移的特征是黏附分子和趋化因子的使用具有冗余性，这使得迄今为止无法进行有效的靶向治疗。此外，在疾病进展过程中，T 细胞进入胰岛并不始终需要同源抗原。然而，髓样细胞是允许 T 细胞和 B 细胞进入胰岛所必需的，并且可能作为控制该过程的途径中的一个汇聚点。在这篇综述中，我们描述了介导 T1D 进展期间免疫细胞向胰岛迁移的因素的现有知识。
