Toxoplasma gondii ROP5 Enhances Type I IFN Responses by Promoting Ubiquitination of STING

文献类型： 外文期刊

第一作者： Jin, Qi-Wang

作者： Jin, Qi-Wang;Yu, Ting;Pan, Ming;Fan, Yi-Min;Ge, Ceng-Ceng;Gong, Jing-Zhi;Tao, Jian-Ping;Huang, Si-Yang;Jin, Qi-Wang;He, Xiao-Bing;Fu, Bao-Quan;Jing, Zhi-Zhong

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关键词： Toxoplasma gondii; ROP5; cGAS-STING pathway; ubiquitination

期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：4.9； 五年影响因子：5.7 ）

ISSN： 1661-6596

年卷期： 2024 年 25 卷 20 期

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收录情况： SCI

摘要： Toxoplasma gondii is a widely spread opportunistic pathogen that can infect nearly all warm-blooded vertebrates and cause serious toxoplasmosis in immunosuppressed animals and patients. However, the relationship between the host's innate immune system and effector proteins is poorly understood, particularly with regard to how effectors antagonize cGAS-STING signaling during T. gondii infection. In this study, the ROP5 from the PRU strain of T. gondii was found to promote cGAS-STING-mediated immune responses. Mechanistically, ROP5 interacted with STING through predicted domain 2 and modulated cGAS-STING signaling in a predicted domain 3-dependent manner. Additionally, ROP5 strengthened cGAS-STING signaling by enhancing the K63-linked ubiquitination of STING. Consistently, ROP5 deficient PRU (PRU Delta ROP5) induced fewer type I IFN-related immune responses and replicated faster than the parental strain in RAW264.7 cells. Taken together, this study provides new insights into the mechanism by which ROP5 regulates T. gondii infection and provides new clues for strategies to prevent and control toxoplasmosis.

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