The absence of IDO upregulates type I IFN production, resulting in suppression of viral replication in the retrovirus-infected mouse

Masato Hoshi, Kuniaki Saito, Akira Hara, Ayako Taguchi, Hirofumi Ohtaki, Ryo Tanaka, Hidetsugu Fujigaki, Yosuke Osawa, Masao Takemura, Hidetoshi Matsunami, Hiroyasu Ito, Mitsuru Seishima

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Indoleamine 2,3-dioxygenase, the L-tryptophan-degrading enzyme, plays a key role in the powerful immunomodulatory effects on several different types of cells. Because modulation of IDO activities after viral infection may have great impact on disease progression, we investigated the role of IDO following infection with LP-BM5 murine leukemia virus. We found suppressed BM5 provirus copies and increased type I IFNs in the spleen from IDO knockout (IDO -/-) and 1-methyl-D-L-tryptophan-treated mice compared with those from wild-type (WT) mice. Additionally, the number of plasmacytoid dendritic cells in IDO-/- mice was higher in the former than in the WT mice. In addition, neutralization of type I IFNs in IDO-/- mice resulted in an increase in LP-BM5 viral replication. Moreover, the survival rate of IDO -/- mice or 1-methyl-D-L-tryptophan-treated mice infected with LP-BM5 alone or with both Toxoplasma gondii and LP-BM5 was clearly greater than the survival rate of WT mice. To our knowledge, the present study is the first report to observe suppressed virus replication with upregulated type I IFN in IDO-/- mice, suggesting that modulation of the IDO pathway may be an effective strategy for treatment of virus infection.

Original languageEnglish
Pages (from-to)3305-3312
Number of pages8
JournalJournal of Immunology
Issue number6
Publication statusPublished - 15-09-2010
Externally publishedYes


All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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