Abstract：
:The mitochondrial antiviral signaling protein (MAVS) mediates the activation of NFkappaB 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 NFkappaB 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.
journal_name
Immunityjournal_title
Immunityauthors
Sun Q,Sun L,Liu HH,Chen X,Seth RB,Forman J,Chen ZJdoi
10.1016/j.immuni.2006.04.004subject
Has Abstractpub_date
2006-05-01 00:00:00pages
633-42issue
5eissn
1074-7613issn
1097-4180pii
S1074-7613(06)00220-2journal_volume
24pub_type
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