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Article Addendum
The non-canonical role of Atg family members as suppressors of innate antiviral immune signaling
Fumihiko Takeshita, Kouji Kobiyama, Atsushi Miyawaki, Nao Jounai and Kenji Okuda
volume 4 | issue 1
1 January 2008Pages: 67 - 69
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Recent research on autophagy clearly demonstrates that the autophagosome-lysosome pathway plays essential roles in elimination of certain pathogens such as group A Streptococcus, Mycobacterium tuberculosis, Listeria monocytogenes, and herpesvirus.1-4 We have recently found that a key regulator of the autophagic process, the Atg12-Atg5 conjugate, associates with the signaling molecules retinoic acid-inducible gene I (RIG-I) and interferon-β promoter stimulator 1 (IPS-1), which are essential for recognition of RNA virus infection and which transmit signals to upregulate type I interferons (IFNs). Interestingly, the Atg12-Atg5 conjugate seemed to negatively regulate the type I IFN modulating pathway through direct interaction with caspase recruitment domains (CARDs) presented by RIG-1 and IPS-1.5 Thus, in contrast to the bactericidal properties of autophagic processes, the autophagy regulator (the Atg12-Atg5 conjugate) appeared to promote RNA virus replication by inhibiting innate anti-virus immune responses. In this addendum, we discuss the non-canonical role of the Atg12-Atg5 conjugate as a suppressor of innate immune responses.
Addendum to: Jounai N, Takeshita F, Kobiyama K, Sawano A, Miyawaki A, Xin KQ, Ishii KJ, Kawai T, Akira S, Suzuki K, Okuda K. The Atg5-Atg12 conjugate associates with innate antiviral immune responses. Proc Natl Acad Sci 2007;104:14050-5
Authors
Fumihiko Takeshita
Yokohama City University Graduate School of Medicine
Kouji Kobiyama
Yokohama City University Graduate School of Medicine
Atsushi Miyawaki
Institute of Physical and Chemical Research (RIKEN)
Nao Jounai
Yokohama City University Graduate School of Medicine
Kenji Okuda
Yokohama City University Graduate School of Medicine
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.