CD8+ T cell-mediated skin disease in mice lacking IRF-2, the transcriptional attenuator of interferon-α/β signaling
CD8+ T cell-mediated skin disease in mice lacking IRF-2, the transcriptional attenuator of interferon-α/β signaling
复制标题
DOI：
10.1016/s1074-7613(00)00064-9
复制
发表时间：
2000-11-01
期刊：
影响因子：
32.4
通讯作者：
Taniguchi, T
中科院分区：
文献类型：
--
作者：
Hida, S;Ogasawara, K;Taniguchi, T
细胞因子的平衡作用被认为是维持体内平衡免疫反应的关键。在这里，我们报告了在缺乏转录因子干扰素调节因子-2 （IRF-2）的小鼠中，涉及CD8(+) T细胞的炎症性皮肤病的发展。CD8(+) T细胞在体外表现出对抗原刺激的高反应性，并伴有干扰素- α / β (ifn - α / β)诱导的基因表达的显著上调。此外，通过引入正向调节ifn - α / β信号通路的基因，疾病发展和CD8(+) T细胞异常都受到抑制。IRF-2可能是一种独特的负调节因子，可以减弱ifn - α / β诱导的基因转录，这对于平衡免疫系统中ifn - α / β信号的有益和有害作用是必要的。
The balanced action of cytokines is known to be critical for the maintenance of homeostatic immune responses. Here, we report the development of an inflammatory skin disease involving CD8(+) T cells, in mice lacking the transcription factor, interferon regulatory factor-2 (IRF-2). CD8(+) T cells exhibit in vitro hyperresponsiveness to antigen stimulation, accompanied with a notable upregulation of the expression of genes induced by interferon-alpha/beta (IFN-alpha/beta). Furthermore, both disease development and CD8(+) T cell abnormality are suppressed by the introduction of nullizygosity to the genes that positively regulate the IFN-alpha/beta signaling pathway. IRF-2 may represent a unique negative regulator, attenuating IFN-alpha/beta -induced gene transcription, which is necessary for balancing the beneficial and harmful effects of IFN-alpha/beta signaling in the immune system.