University of California San Diego, Division of Biology, 9500 Gilman Drive, La Jolla, CA 92093-0377, United States.
Curr Opin Immunol. 2013 Oct;25(5):660-6. doi: 10.1016/j.coi.2013.09.004. Epub 2013 Oct 1.
Upon infection, CD8(+) T cells proliferate and differentiate into armed effector cells capable of eliminating the assaulting pathogen. Although the majority of the antigen-specific T cells will die as the immune response wanes, a few will survive indefinitely to establish the memory population and provide long-lived protection against reinfection. E protein transcription factors and their inhibitors, ID proteins, operate to balance expression of genes that control CD8(+) T cell differentiation through this process. Here, we discuss the role of ID2 and ID3 in promoting the generation and survival of effector and memory populations, particularly highlighting their reciprocal roles in shaping the CD8(+) T cell response unique to the inflammatory milieu. We further examine this coordinated control of gene expression in the context of additional transcription factors within the transcriptional network that programs CD8(+) effector and memory T cell differentiation.
感染后,CD8(+) T 细胞增殖并分化为具有消除侵袭病原体能力的武装效应细胞。尽管随着免疫反应的减弱,大多数抗原特异性 T 细胞将死亡,但少数细胞将无限期存活以建立记忆群体并提供针对再感染的长期保护。E 蛋白转录因子及其抑制剂 ID 蛋白通过这一过程来平衡控制 CD8(+) T 细胞分化的基因的表达。在这里,我们讨论了 ID2 和 ID3 在促进效应细胞和记忆细胞群体的产生和存活中的作用,特别是强调了它们在塑造炎症环境中独特的 CD8(+) T 细胞反应中的相互作用。我们进一步研究了在转录网络内的其他转录因子的背景下,这种基因表达的协调控制,这些转录因子编程 CD8(+)效应和记忆 T 细胞分化。