Agaisse Hervé, Petersen Ulla Maja, Boutros Michael, Mathey-Prevot Bernard, Perrimon Norbert
Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.
Dev Cell. 2003 Sep;5(3):441-50. doi: 10.1016/s1534-5807(03)00244-2.
To characterize the features of JAK/STAT signaling in Drosophila immune response, we have identified totA as a gene that is regulated by the JAK/STAT pathway in response to septic injury. We show that septic injury triggers the hemocyte-specific expression of upd3, a gene encoding a novel Upd-like cytokine that is necessary for the JAK/STAT-dependent activation of totA in the Drosophila counterpart of the mammalian liver, the fat body. In addition, we demonstrate that totA activation also requires the NF-KB-like Relish pathway, indicating that fat body cells integrate the activity of NF-KB and JAK/STAT signaling pathways upon immune response. This study reveals that, in addition to the pattern recognition receptor-mediated NF-KB-dependent immune response, Drosophila undergoes a complex systemic response that is mediated by the production of cytokines in blood cells, a process that is similar to the acute phase response in mammals.
为了表征果蝇免疫反应中JAK/STAT信号通路的特征，我们已将totA鉴定为一个受JAK/STAT通路调控以应对败血症损伤的基因。我们发现，败血症损伤会触发upd3在血细胞中的特异性表达，upd3是一个编码新型Upd样细胞因子的基因，在果蝇相当于哺乳动物肝脏的脂肪体中，该基因对于totA的JAK/STAT依赖性激活是必需的。此外，我们证明totA的激活还需要NF-κB样Relish通路，这表明脂肪体细胞在免疫反应时整合了NF-κB和JAK/STAT信号通路的活性。这项研究表明，除了模式识别受体介导的NF-κB依赖性免疫反应外，果蝇还会经历一种复杂的全身反应，该反应由血细胞中细胞因子的产生介导，这一过程类似于哺乳动物的急性期反应。
Zotero 插件