The Specific and Essential Role of MAVS in Antiviral Innate Immune Responses

Qinmiao Sun, Lijun Sun, Hong Hsing Liu, Xiang Chen, Rashu B. Seth, James Forman, Zhijian J. Chen

Research output: Contribution to journalArticle

406 Scopus citations

Abstract

The mitochondrial antiviral signaling protein (MAVS) mediates the activation of NFκB and IRFs and the induction of interferons in response to viral infection. In vitro studies have also suggested that MAVS is required for interferon induction by cytosolic DNA, but the in vivo evidence is lacking. By generating MAVS-deficient mice, here we show that loss of MAVS abolished viral induction of interferons and prevented the activation of NFκB and IRF3 in multiple cell types, except plasmacytoid dendritic cells (pDCs). However, MAVS was not required for interferon induction by cytosolic DNA or by Listeria monocytogenes. Mice lacking MAVS were viable and fertile, but they failed to induce interferons in response to poly(I:C) stimulation and were severely compromised in immune defense against viral infection. These results provide the in vivo evidence that the cytosolic viral signaling pathway through MAVS is specifically required for innate immune responses against viral infection.

Original languageEnglish (US)
Pages (from-to)633-642
Number of pages10
JournalImmunity
Volume24
Issue number5
DOIs
StatePublished - May 1 2006

Keywords

  • MICROBIO
  • MOLIMMUNO
  • SIGNALING

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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