TRIM29 Negatively Regulates the Type I IFN Production in Response to RNA Virus

The Journal of Immunology : Official Journal of the American Association of Immunologists
Junji XingZhiqiang Zhang

Abstract

The innate immunity is critically important in protection against virus infections, and in the case of RNA viral infections, the signaling mechanisms that initiate robust protective innate immunity without triggering autoimmune inflammation remain incompletely defined. In this study, we found the E3 ligase TRIM29 was specifically expressed in poly I:C-stimulated human myeloid dendritic cells. The induced TRIM29 played a negative role in type I IFN production in response to poly I:C or dsRNA virus reovirus infection. Importantly, the challenge of wild-type mice with reovirus led to lethal infection. In contrast, deletion of TRIM29 protected the mice from this developing lethality. Additionally, TRIM29-/- mice have lower titers of reovirus in the heart, intestine, spleen, liver, and brain because of elevated production of type I IFN. Mechanistically, TRIM29 was shown to interact with MAVS and subsequently induce its K11-linked ubiquitination and degradation. Taken together, TRIM29 regulates negatively the host innate immune response to RNA virus, which could be employed by RNA viruses for viral pathogenesis.

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Citations

Jul 5, 2019·The Journal of Immunology : Official Journal of the American Association of Immunologists·Yaling DouZhiqiang Zhang
Oct 30, 2019·The Journal of General Virology·Adam Hage, Ricardo Rajsbaum
Jun 11, 2019·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Wenjiao LiXuan Cao
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Jan 20, 2021·Cellular & Molecular Immunology·Koji OnomotoMitsutoshi Yoneyama
Oct 30, 2020·Frontiers in Immunology·Wenyong YangHongbo Hu
Jan 7, 2021·Cellular & Molecular Biology Letters·Michal Tracz, Wojciech Bialek
Jun 24, 2021·Cell Reports·Junji XingZhiqiang Zhang

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