IL-33/ST2轴作为众所周知的抗结核内源性防御

M. Karbalaei, K. Ghazvini, M. Keikha
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引用次数: 0

摘要

感染是由一种细胞内细菌结核分枝杆菌引起的。该疾病是最重要的传染病之一,在世界范围内,其发病率和死亡率最高。卫生组织年的全球报告显示,从2018年的1070万感染者中,有160万人死亡。尽管BCG疫苗已经使用了大约一百年,但它只对儿童有效,但无法对成人肺结核产生保护性和可靠的免疫力。因此,使用比BCG更高效的替代疫苗似乎是当务之急。IL-33/ST2轴形成IL-33和ST2,它们都是IL-1家族的成员。IL-33被分泌作为对细胞应激的警报,ST2引起MyD88/NF-κB信号通路的刺激,这是感染细胞对Mtb和其他细胞内病原体的适当反应所必需的。在Th2细胞中,NF-κB进入细胞核,并作为转录因子发挥作用。最后,细胞因子如
本文章由计算机程序翻译,如有差异,请以英文原文为准。
IL-33/ST2 Axis as a Well-Known Endogenous Defense Against Tuberculosis
infection is caused by an intracellular bacterium, Mycobacterium tuberculosis (Mtb). The disease is among the most important infectious diseases, which has dedicated most cases of morbidity and mortality to itself worldwide. The global report of Health Organization in shows that from 10.7 million infected people in 2018, 1.6 million died. Although the BCG vaccine has been used for about a hundred years, it is only effective in children, but is not able to produce a protective and reliable immunity against adult pulmonary TB. Hence, using an alternative vaccine with high more efficacy than BCG seems to be urgent. The IL-33/ST2 axis forms of IL-33 and ST2, and both of them are the members of IL-1 family. IL-33 is secreted as an alarm in response to cellular stress, and ST2 causes stimulation of MyD88/NF-κB signaling pathway, which is needed for the proper response of infected cells to Mtb and other intracellular pathogens. In Th2 cells, NF-κB enters into the nucleus, and acts as a transcription factor. Finally, cytokines such as effective in the
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