Sullivan Brandon M, Juedes Amy, Szabo Susanne J, von Herrath Matthias, Glimcher Laurie H
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Harvard Medical School, Boston, MA 02115, USA.
Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15818-23. doi: 10.1073/pnas.2636938100. Epub 2003 Dec 12.
Type 1 immunity relies on the differentiation of two major subsets of T lymphocytes, the CD4+ T helper (Th) cell and the CD8+ cytotoxic T cell, that direct inflammatory and cytotoxic responses essential for the destruction of intracellular and extracellular pathogens. In contrast to CD4 cells, little is known about transcription factors that control the transition from the CD8 naïve to effector cell stage. Here, we report that the transcription factor T-bet, known to regulate Th cell differentiation, also controls the generation of the CD8+ cytotoxic effector cell. Antigen-driven generation of effector CD8+ cells was impaired in OT-I T cell receptor transgenic mice lacking T-bet, resulting in diminished cytotoxicity and a marked shift in cytokine secretion profiles. Furthermore, mice lacking T-bet responded poorly to infection with lymphocytic choriomeningitis virus. T-bet is a key player in the generation of type 1 immunity, in both Th and T cytotoxic cells.
1型免疫依赖于两类主要的T淋巴细胞亚群的分化,即CD4 +辅助性T细胞(Th细胞)和CD8 +细胞毒性T细胞,它们指导对细胞内和细胞外病原体破坏至关重要的炎症和细胞毒性反应。与CD4细胞不同,对于控制从CD8幼稚细胞向效应细胞阶段转变的转录因子了解甚少。在这里,我们报告称,已知调节Th细胞分化的转录因子T-bet,也控制CD8 +细胞毒性效应细胞的产生。在缺乏T-bet的OT-I T细胞受体转基因小鼠中,抗原驱动的效应性CD8 +细胞的产生受损,导致细胞毒性降低以及细胞因子分泌谱明显改变。此外,缺乏T-bet的小鼠对淋巴细胞性脉络丛脑膜炎病毒感染反应不佳。T-bet在Th细胞和细胞毒性T细胞的1型免疫产生中均起着关键作用。