Research Campus of the Friedrich-Alexander University Erlangen-Nuernberg, Medical Clinic I, 91052, Erlangen, Germany.
Curr Diab Rep. 2012 Oct;12(5):463-70. doi: 10.1007/s11892-012-0295-2.
Foxp3(+) regulatory T (Treg) cells serve as a vital mechanism of negative regulation to maintain immunological self-tolerance thereby suppressing immune-mediated inflammation. The identification of the transcription factor Foxp3 as the specification factor for the Treg cell lineage facilitated our understanding in the biology of Treg generation and function. In the past, we carefully studied the extrathymic conversion of naive CD4(+) T cells into Foxp3(+) expressing Treg cells and found that this process is most efficient upon subimmunogenic supply of strong-agonistic T cell receptor (TCR) ligands avoiding activation of antigen-presenting and T cells. In contrast, weak-agonistic antigens fail to efficiently induce stable Foxp3(+) Treg cells irrespective of the applied dose. Here, we discuss the specific requirements for the establishment of Treg vaccination protocols to interfere with autoimmunity such as Type 1 diabetes.
Foxp3(+) 调节性 T (Treg) 细胞作为一种重要的负调控机制，有助于维持免疫耐受，从而抑制免疫介导的炎症。转录因子 Foxp3 作为 Treg 细胞谱系的特异性因子，促进了我们对 Treg 细胞生成和功能的生物学理解。过去，我们仔细研究了幼稚 CD4(+) T 细胞在外周向 Foxp3(+)表达 Treg 细胞的转化，发现该过程在外源给予低剂量的强效 T 细胞受体 (TCR) 配体时效率最高，从而避免了抗原呈递细胞和 T 细胞的激活。相比之下，弱激动性抗原即使应用较高剂量也不能有效地诱导稳定的 Foxp3(+) Treg 细胞。在此，我们讨论了建立 Treg 疫苗接种方案以干预自身免疫性疾病（如 1 型糖尿病）的具体要求。
