Mozer-Lisewska Iwona, Kaczmarek Mariusz, Zeromski Jan
Klinika Chorób Zakaźnych i Neurologii Dzieciqcej III Katedry Pediatrii Akademii Medycznej im. Karola Marcinkowskiego, Poznań.
Postepy Biochem. 2006;52(1):56-61.
Essential data pertaining to the structure and function of selected transcription factors such as NFAT, AP-1 and NF-kappaB in particular, are presented in the relation to viral hepatitis C and B. In chronic hepatitis C the activation of NF-kappaB is markedly modulated by viral proteins such as core protein and nonstructural ones, particularly NS5A and NS3. In hepatitis B the major factor influencing NF-kappaB function appears to be HBx protein. Effects of viral proteins on NF-kappaB function in relation to the course of hepatitis are complex. They participate in the perpetuation of inflammatory state in the liver, inhibit apoptosis of hepatocytes, as well as the differentiation of antigen-presenting cells (dendritic ones). The latter effect has deleterious impact on the formation of specific immune response to viral peptides. It seems that both viruses, C and B acquired the ability to modify NF-KB function in advantage for the pathogens in question.
本文特别介绍了与某些转录因子(如活化T细胞核因子、活化蛋白-1和核因子κB)的结构和功能相关的重要数据,这些数据与丙型和乙型病毒性肝炎有关。在慢性丙型肝炎中,核因子κB的激活受到病毒蛋白(如核心蛋白和非结构蛋白,特别是NS5A和NS3)的显著调节。在乙型肝炎中,影响核因子κB功能的主要因素似乎是乙肝x蛋白。病毒蛋白对核因子κB功能的影响与肝炎病程相关,情况较为复杂。它们参与肝脏炎症状态的持续,抑制肝细胞凋亡以及抗原呈递细胞(树突状细胞)的分化。后一种作用对针对病毒肽的特异性免疫反应的形成具有有害影响。丙型和乙型这两种病毒似乎都获得了改变核因子κB功能的能力,这对相关病原体有利。