MEK/ERK MAP kinase limits poly I:C-induced antiviral gene expression in RAW264.7 macrophages by reducing interferon-beta expression

FEBS Letters

article

Shawn M. Freed¹  Danielle S. Baldi¹  Jason A. Snow¹  Sierra R. Athen¹  Zachary P. Guinn²  T. Scott Pinkerton¹  Thomas M. Petro²  Tyler C. Moore¹ 

[1] Department of Biology, College of Science and Technology, Bellevue University;Department of Oral Biology, College of Dentistry, University of Nebraska Medical Center, Lincoln

关键词: EGFR;    ERK;    interferon;    IRF3;    ISG;    poly I:C;    RAW264.7;    TLR3;   

DOI  :  10.1002/1873-3468.14200

来源: John Wiley & Sons Ltd.

【 摘 要 】

Toll-like receptor 3 (TLR3) recognizes viral double-stranded RNA (or the synthetic dsRNA analog poly I:C) and induces a signal transduction pathway that results in activation of transcription factors that induce expression of antiviral genes including type I interferon (IFN-I). Secreted IFN-I positively feeds back to amplify antiviral gene expression. In this report, we study the role of MEK/ERK MAP kinase in modulating antiviral gene expression downstream of TLR3. We find MEK/ERK is a negative regulator of antiviral gene expression by limiting expression of IFN-β. However, MEK/ERK does not limit antiviral responses downstream of the type I interferon receptor. These findings provide insights into regulatory mechanisms of antiviral gene expression and reveal potential targets for modulating antiviral immunity.

【 授权许可】

Unknown