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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.

Author information

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

Abstract

Background:

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.

Results:

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.

Conclusions:

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.

KEYWORDS:

Antiviral immunity; TRAF2; TRAF3; Type I interferon

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