2018 Fiscal Year Annual Research Report
Molecular mechanisms for IgA-mediated regulations of host-microbiota symbiosis
Project/Area Number |
16H02632
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Research Institution | Institute of Physical and Chemical Research |
Principal Investigator |
ファガラサン シドニア 国立研究開発法人理化学研究所, 生命医科学研究センター, チームリーダー (00391970)
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Co-Investigator(Kenkyū-buntansha) |
服部 正平 早稲田大学, 理工学術院, 教授(任期付) (70175537)
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Project Period (FY) |
2016-04-01 – 2019-03-31
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Keywords | Immunology / IgA |
Outline of Annual Research Achievements |
We previously demonstrated that gut IgAs contribute to regulating the gut bacterial communities, but the mechanisms involved in such regulation remained unknown. We speculated that not only the repertoire but also the post-translational modifications might be different between IgAs elicited in different conditions (for example non-selected or “default” IgA versus adaptive, selected or “homeostatic” IgA). Thus we analyzed the properties of IgA from genetically modified mice lacking germinal centers, such as T cell deficient mice, or germ-free (GF) mice as well as gnotobiotic mice. We found that the “default” IgAs were heavily glycosylated and that the addition of bacteria drastically modified the sugar contents of IgAs. Sequencing analyses of bacteria coated with different IgA qualities will be analyzed in collaboration with the group of Professor Hattori. Furthermore, different bacterial species generated different glycosylation profiles, implicating that not only the immune system but also the microbiota contribute to biochemical characteristics of IgA in the gut. We began to dissect the importance of such post-translational modifications of IgA in the contexts of symbiotic interactions. The studies will be continued in the coming years. We believe that such fundamental research will contribute to deeper understanding of the basic principles governing the homeostasis at the mucosal surface. It will also allow envisioning strategies aiming to restore homeostasis in diseases accompanied by changes in microbiota composition and function.
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Research Progress Status |
平成30年度が最終年度であるため、記入しない。
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Strategy for Future Research Activity |
平成30年度が最終年度であるため、記入しない。
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Research Products
(2 results)