ニシオ　ジュンコ   Nishio Junko   西尾　純子    所属   東邦大学  医学部 医学科    職種   准教授
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Cross-interference of RLR and TLR signaling pathways modulates antibacterial T cell responses.
掲載誌名	正式名：Nature immunology
掲載区分	国外
巻・号・頁	13(7),pp.659-66
著者・共著者	Hideo Negishi,Hideyuki Yanai,Akira Nakajima,Ryuji Koshiba,Koji Atarashi,Atsushi Matsuda,Kosuke Matsuki,Shoji Miki,Takahiro Doi,Alan Aderem,Junko Nishio,Stephen T Smale,Kenya Honda,Tadatsugu Taniguchi
発行年月	2012/05/20
概要	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.
DOI	10.1038/ni.2307
PMID	22610141