2017 Fiscal Year Final Research Report
Anti-inflammatory mechanism from small intestine to whole body via interferon-beta
Project/Area Number |
15H04504
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Food science
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Research Institution | National Institute of Advanced Industrial Science and Technology |
Principal Investigator |
Tsuji Noriko 国立研究開発法人産業技術総合研究所, 生命工学領域, 上級主任研究員 (30343990)
|
Co-Investigator(Kenkyū-buntansha) |
平山 和宏 東京大学, 大学院農学生命科学研究科(農学部), 准教授 (60208858)
角田 茂 東京大学, 医科学研究所, 助教 (80345032)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | lactic acid bacteria / intreferon-beta / small intestine / anti-inflammation / dendritic cell / Peyer's patch / Th1 / oral tolerance |
Outline of Final Research Achievements |
Double-stranded RNA of lactic acid bacteria (LAB) is recognized by dendritic cells (DCs) via endosomal-TLR3 and benefits the anti-inflammatory response through induction of interferon-β (IFN-β). However, how such IFN-β impacts T cell immune responses, and how immune homeostasis is better maintained in the presence of commensal or food-derived LAB was unknown. Here we show that LAB enhances interleukin-12 (IL-12) secretion by DCs and differentiation of IFN-γ-producing T cells in an IFN-β-dependent manner. We demonstrated that IFN-β secreted in response to LAB increased IFN regulatory factor 1 (IRF1) and IRF7 mRNA, which contribute to Il12p35 expression. We clarified the DC subset in Peyer’s patches that induce Th1 cell differentiation through IFN-β production in response to LAB. Th1 polarization and maintenance of Foxp3 expression by CD4+ T cells due to TLR3-mediated IFN-β production may thus confer anti-allergic or anti-inflammatory activity by commensal or probiotic LAB.
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Free Research Field |
Mucosal Immunology
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