Journal
NATURE IMMUNOLOGY
Volume 13, Issue 7, Pages 659-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2307
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Funding
- Ministry of Education, Culture, Sports, Science, and Technology of Japan
- Japan Science and Technology Agency (Core Research for Evolutional Science and Technology)
- Japan Society for the Promotion of Science
- Grants-in-Aid for Scientific Research [22114007, 24590574] Funding Source: KAKEN
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Although the mechanisms by which innate pathogen-recognition receptors enhance adaptive immune responses are increasingly well understood, whether signaling events from distinct classes of receptors affect each other in modulating adaptive immunity remains unclear. We found here that the activation of cytosolic RIG-I-like receptors (RLRs) resulted in the selective suppression of transcription of the gene encoding the p40 subunit of interleukin 12 (Il12b) that was effectively induced by the activation of Toll-like receptors (TLRs). The RLR-activated transcription factor IRF3 bound dominantly, relative to IRF5, to the Il12b promoter, where it interfered with the TLR-induced assembly of a productive transcription-factor complex. The activation of RLRs in mice attenuated TLR-induced responses of the T helper type 1 cell (T(H)1 cell) and interleukin 17-producing helper T cell (T(H)17 cell) subset types and, consequently, viral infection of mice caused death at sublethal doses of bacterial infection. The innate immune receptor cross-interference we describe may have implications for infection-associated clinical episodes.
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