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鉴定了严重病毒性肝炎的细胞机制 [复制链接]

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发表于 2018-1-19 13:47 |只看该作者 |倒序浏览 |打印
                    Cellular mechanism for severe viral hepatitis identified                                                

The Korea Advanced Institute of Science and Technology (KAIST)

   

            
  
  
                              
      IMAGE: Treg cells from acute hepatitis A (AHA) patients produce tumor necrosis factor (TNF) andhave reduced suppressive activity. These changes are due to a decrease in FoxP3 transcription factor and an...       view more
   

Credit: KAIST

                  KAIST medical scientists identified a cellular mechanism causing inflammatory changes in regulatory T cells that can lead to severe viral hepatitis. Research on this mechanism will help further understand the nature of various inflammatory diseases and lead to the development of relevant clinical treatments.
         It is known that activated immune cells of patients with viral hepatitis destroy hepatocyte, but its regulatory mechanism has not yet been described.
         Regulatory T cells inhibit activation of other immune cells and thus are important for homeostasis of the immune system. However, recent studies contradictorily show that immune inhibitory functions of regulatory T cells weaken in inflammatory conditions and the cells secrete inflammatory cytokines in response. Meanwhile, such a phenomenon was not observed in viral hepatitis including types A, B and C.
         The team focused on changes in regulatory T cells in patients with viral hepatitis and discovered that regulatory T cells undergo inflammatory changes to secrete inflammatory cytokines (protein secreted by immune cells) called TNF. They also proved regulatory T cells that secrete TNF contribute to the progression of viral hepatitis.
         The team confirmed that regulatory T cells of acute hepatitis A patients have reduced immune-inhibitory functions. Instead, their regulatory T cells secrete TNF. Through this research, the team identified a molecular mechanism for changes in regulatory T cells and identified the transcription factor regulating the process. Furthermore, the team found similar changes to be also present in hepatitis B and C patients.
         A KAIST immunology research team led by Professors Eui-Cheol Shin and Min Kyung Jung at the Graduate School of Medical Science & Engineering conducted this translational research with teams from Chungnam National University and Yonsei University to identify the mechanism in humans, instead of using animal models. The research was described in Gastroenterology last December.
         Professor Shin said, "This is the first research on regulatory T cells that contributes to hepatocyte damage in viral hepatitis." He continued, "It is significant for identifying the cells and the molecules that can be used as effective treatment targets for viral hepatitis in the future. This research was funded by the Samsung Science and Technology Foundation.

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发表于 2018-1-19 13:48 |只看该作者
鉴定了严重病毒性肝炎的细胞机制

韩国科学技术高等研究院(KAIST)
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IMAGE:急性甲型肝炎(AHA)患者的Treg细胞产生肿瘤坏死因子(TNF)并具有降低的抑制活性。这些变化是由于FoxP3转录因子的减少和...查看更多

学分:KAIST

KAIST医学科学家发现了导致调节性T细胞发生炎症变化的细胞机制,导致严重的病毒性肝炎。对这一机制的研究将有助于进一步了解各种炎症性疾病的性质,并导致相关临床治疗的发展。

已知病毒性肝炎患者的活化免疫细胞破坏肝细胞,但其调节机制尚未描述。

调节性T细胞抑制其他免疫细胞的活化,因此对于免疫系统的稳态是重要的。然而,最近的研究相反地表明,调节性T细胞的免疫抑制功能在炎性条件下减弱,细胞分泌炎性细胞因子作为应答。同时,在包括A,B和C型的病毒性肝炎中未观察到这种现象。

该研究小组专注于病毒性肝炎患者调节性T细胞的变化,并发现调节性T细胞发生炎性改变,分泌炎性细胞因子(由免疫细胞分泌的蛋白质),称为TNF。他们还证明分泌TNF的调节性T细胞有助于病毒性肝炎的进展。

研究小组证实急性甲型肝炎患者的调节性T细胞具有降低的免疫抑制功能。相反,它们的调节性T细胞分泌TNF。通过这项研究,小组确定了调节性T细胞变化的分子机制,并确定了调节过程的转录因子。此外,研究小组发现乙肝和丙肝患者也有类似的变化。

由医学科学研究生院的Eui-Cheol Shin和Min Kyung Jung教授领导的KAIST免疫学研究小组与忠南大学和延世大学的研究小组一起进行了这一转化研究,以确定人类的机制,而不是使用动物模型。该研究在去年12月的胃肠病学中被描述。

Shin教授说:“这是第一个调节性T细胞的研究,这种调节性T细胞对病毒性肝炎的肝细胞损伤有贡献。”他继续说:“确定可用作未来病毒性肝炎有效治疗靶点的细胞和分子具有重要意义。本研究由三星科技基金会资助。

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发表于 2018-1-19 14:25 |只看该作者
调节性T细胞是未来生物科技主力!
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