Takeda K, Akira S
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.
Jpn J Infect Dis. 2001 Dec;54(6):209-19.
Innate immune response in Drosophila is mediated by signaling through Toll receptors. In mammals, Toll-like receptors (TLRs), comprising a large family, recognize a specific pattern of microbial components. So far, the roles of TLR2, TLR4, TLR5, TLR6, and TLR9 have been revealed. The recognition of microbial components by TLRs leads to activation of innate immunity, which provokes inflammatory responses and finally the development of adaptive immunity. The inflammatory response depends on a TLR-mediated MyD88-dependent cascade. However, there seems to exist additional cascades in TLR signaling. In the case of TLR4 signaling, an MyD88-independent pathway is now being characterized. In addition to the activation of innate immune responses, TLR-mediated signaling leads to suppression of the activity of innate immune cells, represented by "lipopolysaccharide (LPS) tolerance". Progress in elucidating the molecular mechanisms for LPS tolerance has been made through the analysis of TLR-mediated signaling pathways. Thus, the activity for innate immune responses is known to be finely regulated by TLRs.
果蝇中的固有免疫反应是通过Toll受体介导的信号传导来实现的。在哺乳动物中，Toll样受体（TLR）构成一个大家族，可识别特定模式的微生物成分。到目前为止，TLR2、TLR4、TLR5、TLR6和TLR9的作用已经被揭示。TLR对微生物成分的识别会导致固有免疫的激活，进而引发炎症反应并最终促进适应性免疫的发展。炎症反应依赖于TLR介导的MyD88依赖性级联反应。然而，TLR信号传导中似乎还存在其他级联反应。就TLR4信号传导而言，一条不依赖MyD88的途径目前正在被阐明。除了激活固有免疫反应外，TLR介导的信号传导还会导致以“脂多糖（LPS）耐受”为代表的固有免疫细胞活性受到抑制。通过对TLR介导的信号通路进行分析，在阐明LPS耐受的分子机制方面已经取得了进展。因此，已知固有免疫反应的活性受到TLR的精细调节。
