Immunity:病毒如何绕过免疫系统,引发慢性感染?
2018/02/10
包括HIV、HCV等在内的病毒是如何战胜免疫系统引发慢性感染的呢?这一直是个未解之谜。近期,来自于麦吉尔大学的科学家们给出了新线索,他们发现了病毒“干扰”免疫细胞的分子机制,有望成为解决谜团的关键。


图片来源:网络

通常,免疫系统会快速识别、消灭入侵的病原体,而CD8+ T细胞是行使这一职责的“主力军”。大多数情况下,T细胞会接受细胞因子的“指令”,从而快速识别并摧毁感染细胞,以防止感染扩散。

“但是,面对慢性感染时,免疫细胞会接收到错误的‘指示’,其防御能力会减弱。” 麦吉尔大学微生物与免疫学助理教授、文章通讯作者Martin Richer带领团队发现了这背后的关键机制,相关研究成果发表在《Immunity》期刊。


图片来源:Immunity(DOI: https://doi.org/10.1016/j.immuni.2018.01.006)

他们发现,某些病毒之所以能够在体内存活,是因为它们通过驱动细胞因子,修改CD8+T细胞表面的糖蛋白,从而减弱其免疫能力。

这一策略减弱了免疫细胞的抗原敏感度,为病毒入侵赢得时间,从而使其能够绕过免疫防御,最终造成慢性感染。研究人员认为,靶向这一机制,有望恢复T细胞的部分功能,从而增强机体对抗感染的能力。


慢性感染病毒抵抗的细节(图片来源:Immunity

“我们可以利用这些信号通路,增强免疫系统的灵敏性,从而找到治疗慢性感染的新方法。这一发现对于癌症、自身免疫类疾病也有一定的意义。” Richer强调道。

参考资料:

How viruses disarm the immune system

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  • Interleukin-10 Directly Inhibits CD8+ T Cell Function by Enhancing N-Glycan Branching to Decrease Antigen Sensitivity

    Chronic viral infections remain a global health concern. The early events that facilitate viral persistence have been linked to the activity of the immunoregulatory cytokine IL-10. However, the mechanisms by which IL-10 facilitates the establishment of chronic infection are not fully understood. Herein, we demonstrated that the antigen sensitivity of CD8+ T cells was decreased during chronic infection and that this was directly mediated by IL-10. Mechanistically, we showed that IL-10 induced the expression of Mgat5, a glycosyltransferase that enhances N-glycan branching on surface glycoproteins. Increased N-glycan branching on CD8+ T cells promoted the formation of a galectin 3-mediated membrane lattice, which restricted the interaction of key glycoproteins, ultimately increasing the antigenic threshold required for T cell activation. Our study identified a regulatory loop in which IL-10 directly restricts CD8+ T cell activation and function through modification of cell surface glycosylation allowing the establishment of chronic infection.

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