| セッション情報 |
Poster Presentation(GI)
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| タイトル |
IF-P1-6 Maintenance of Colonic Homeostasis by Distinct Toll-like Receptor Signaling
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| 演者 |
Kyoko Katakura（Department of Gastroenterology and RheumatologySchool of MedicineFukushima Medical UniversityJapan） |
| 共同演者 |
Ryoma Suzuki（Department of Gastroenterology and RheumatologySchool of MedicineFukushima Medical UniversityJapan）, Tatsuo Fujiwara（Department of Gastroenterology and RheumatologySchool of MedicineFukushima Medical UniversityJapan）, Naohiko Gunji（Department of Gastroenterology and RheumatologySchool of MedicineFukushima Medical UniversityJapan）, Hiromasa Ohira（Department of Gastroenterology and RheumatologySchool of MedicineFukushima Medical UniversityJapan） |
| 抄録 |
Toll－like receptors （TLRs） are crucial sensors of the innate immune system that recognize signature mi－crobial compounds． Although intestinal microbiota prQvokes intestinal inflammationwe have previouslydemonstrated that activation of TLR9 by commensal bacteria also has an essential role in maintainingcolonic homeostasis． The abnormal innate immune responses toward luminal bacteria would play an im－portant role in廿しe pathogenesis of inflammatory bowel disease（正の）．Herewe preseIlt several effects ofTLR signaling towards mouse intestinal inflammation． ln case of TLR4we proved that repeated TLR4 ag－onistlipopolysaccharide （LPS）administration could protect colonic inflammation of mouse experimentalcolitis modeL This phenomenon originated from LPS tolerance and IRAK－Mnegative regulator of TLRsignalingwas a great participant． TLR7 agonist Imiquimod（工MQ）has been commercially teste dandsame as TLR9 ligandagonistic stimulation of TLR7 in plasmacytoid dendritic cells （pDCs） results in type－1 IFN production． We could find that IMQ protects mice from colonic infiaimnation through induction ofregulatory T cells （Tregs） ． Previous report showe・d that TLR9 stimulated maturing pDC have an intrinsicproperty to mhibit immune responses by inducing IL－10producing Tregs when directly presenting anti－gen to T cells． Therefore we considered same mechanism underlying TLR 7 ／mediated anti－inflammatoryeffect ln conclusionour mouse studies of TLR responses in the gut indicate that TLR signaling orches－trated several immune cells and moleculesthereby controlling colonic inflammation and tolerance． |
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