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在系统性淋巴细胞膜炎病毒感染期间,ISG15驱动免疫病理和呼吸系统衰竭

Namir Shaabani¹, Jaroslav Zak¹, Jennifer L Johnson²

¹Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA.

Journal of immunology (Baltimore, Md. : 1950)

|November 4, 2024

概括

病毒感染期间USP18酶功能缺乏会导致严重的免疫病理. 失调的ISG15信号导致致命的结果,这表明它是严重病毒感染的治疗目标.

科学领域:

免疫学免疫学免疫学
病毒学病毒学
病理学病理学病理学

背景情况:

干扰素刺激基因15 (ISG15) 对于抗病毒免疫非常重要,但在持久性感染中可能导致病理.
了解ISG15的双重作用对于开发针对病毒性疾病的疗法至关重要.

研究的目的:

研究USP18酶功能和ISG15在持续性病毒感染期间免疫病理中的作用.
为了确定严重病毒感染的潜在治疗点.

主要方法:

使用了USP18缺乏的,USP18酶不活的和Isg15缺乏的小鼠模型.
研究了中断ISG15结合/解结合酶的影响 (Uba7, Usp18).
研究了骨髓细胞的作用,并进行了骨髓细胞枯竭.

主要成果:

缺乏USP18酶功能导致严重的病理,包括血液学障碍,肺炎,血管泄漏和死亡.
骨髓细胞特异性Usp18缺乏症模仿了这些病理,需要ISG15.
与ISG15结合/解结合的干扰导致ISG15积累,中性粒细胞透,肺病变和死亡.

结论:

在持续的病毒感染期间,ISG15的失调生产和信号传递可能会导致致命的免疫病理.
针对ISG15信号传输可能有利于治疗肺部表现的严重病毒感染.

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