Institut National de la Santé et de la Recherche Médicale (INSERM) U986, Hôpital Saint Vincent de Paul, Bâtiment Petit, 82 Avenue Denfert-Rochereau, 75014 Paris, France.
Nat Rev Immunol. 2010 Jul;10(7):501-13. doi: 10.1038/nri2787.
The development of type 1 diabetes involves a complex interaction between pancreatic beta-cells and cells of both the innate and adaptive immune systems. Analyses of the interactions between natural killer (NK) cells, NKT cells, different dendritic cell populations and T cells have highlighted how these different cell populations can influence the onset of autoimmunity. There is evidence that infection can have either a potentiating or inhibitory role in the development of type 1 diabetes. Interactions between pathogens and cells of the innate immune system, and how this can influence whether T cell activation or tolerance occurs, have been under close scrutiny in recent years. This Review focuses on the nature of this crosstalk between the innate and the adaptive immune responses and how pathogens influence the process.
1 型糖尿病的发展涉及胰腺β细胞与固有和适应性免疫系统细胞之间的复杂相互作用。对自然杀伤 (NK) 细胞、NKT 细胞、不同树突状细胞群体和 T 细胞之间相互作用的分析强调了这些不同细胞群体如何影响自身免疫的发生。有证据表明,感染在 1 型糖尿病的发展中可能具有增强或抑制作用。近年来,病原体与固有免疫系统细胞之间的相互作用以及这如何影响 T 细胞激活或耐受的发生一直受到密切关注。这篇综述重点介绍了固有免疫和适应性免疫反应之间这种串扰的性质以及病原体如何影响这一过程。