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Cell Biosci. 2019 Jan 3;9:5. doi: 10.1186/s13578-018-0268-5. eCollection 2019.

Cell type-specific function of TRAF2 and TRAF3 in regulating type I IFN induction.

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1Department of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX 77030 USA.
2Life Sciences Institute, Zhejiang University, Hangzhou, 310058 China.
3Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX USA.
4The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030 USA.



TRAF3 is known as a central mediator of type I interferon (IFN) induction by various pattern recognition receptors, but the in vivo function of TRAF3 in host defense against viral infection is poorly defined due to the lack of a viable mouse model.


Here we show that mice carrying conditional deletion of TRAF3 in myeloid cells or dendritic cells do not have a significant defect in host defense against vesicular stomatitis virus (VSV) infection. However, whole-body inducible deletion of TRAF3 renders mice more sensitive to VSV infection. Consistently, TRAF3 was essential for type I IFN induction in mouse embryonic fibroblasts (MEFs) but not in macrophages. In dendritic cells, TRAF3 was required for type I IFN induction by TLR ligands but not by viruses. We further show that the IFN-regulating function is not unique to TRAF3, since TRAF2 is an essential mediator of type I IFN induction in several cell types, including macrophages, DCs, and MEFs.


These findings suggest that both TRAF2 and TRAF3 play a crucial role in type I IFN induction, but their functions are cell type- and stimulus-specific.


Antiviral immunity; TRAF2; TRAF3; Type I interferon

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