Biotechnology Essay代写:炎性因子IL-34
Keywords: Biotechnology Essay代写
几乎很少是目前关于新发现的炎性因子IL-34 IAV感染或发病机制，IAV上调表达的调节称。本研究提供了相当大的新信息有关这些问题。我们ï¬首先确定ï¬，IAV可以上调IL-34表达。然后我们证明了一个以前未知的循环中，IL-22上调IL-34表达和IL-34反馈抑制猪流感病毒感染PBMC IL-22的表达。目前，“'cross-talk”一些重要的促炎因子，与IL-22、IL-6和IFN-α的γ，已经被广泛的研究（Stoyan等人。2013），但IL-22和发病之间的关系进行了评估。 本研究的IAV感染诱导的IL-32水平之间的体外和体内有差别。有超过20倍的增加，感染的细胞培养物或在体外，然而，IL-34 mRNA水平均高约9.9折在IAV的患者比健康人的体内。由于炎症因子相互调节的复杂炎症网络，炎症因子在生理条件下不可能急剧增加。 总之，我们提出了一个假设的模型根据IAV引发IL-22和IL-34生产，导致炎症反应fl主机。在这个模型中，我们进一步发现IL-22位于在正调控通路发病流。如图5所示，两基因之间的串扰如下：IL-22上调IL-34生产，反之，IL-34 IL-22活性减毒。
Biotechnology Essay代写:炎性因子IL-34
In our present study, there was a difference of the IAV infection induced IL-32 level between in vitro and in vivo. There was an over 20-fold increased in cell cultures infected with IAV in vitro, however, IL-34 mRNA levels were approximately 9.9-fold higher in IAV patients than in healthy individuals in vivo. It is likely the inflammatory factor is not able to be increased sharply under physiological conditions due to complex inflammation network in which inflammatory factors regulate each other.
In summary, we proposed a hypothetical model according to which IAV triggered the production of IL-22 and IL-34, resulting in a host inflammatory response. In this model, we further demonstrated that IL-22 was located up-stream of IL-34 in the positive regulatory pathway. As shown in Fig. 5, the cross-talk between the two genes was described as follows: IL-22 upregulated IL-34 production, and conversely, IL-34 attenuated IL-22 activity.
