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KAKEN_23591461seika.pdf
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経口寛容、および食物アレルギーにおけるTh17細胞の役割解明
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| Kana |
ケイコウ カンヨウ, オヨビ ショクモツ アレルギー ニ オケル Th17 サイボウ ノ ヤクワリ カイメイ
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Keiko kanyo, oyobi shokumotsu arerugi ni okeru Th17 saibo no yakuwari kaimei
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Commensal bacteria suppresses food allergy by inhibiting ILC2 cytokine production through the induction of IL-17 producing cells
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中川, 竜介
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ナカガワ, リュウスケ
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Nakagawa, Ryusuke
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慶應義塾大学・医学部・准教授
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Research team head
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科研費研究者番号 : 10360603
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吉村, 昭彦
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ヨシムラ, アキヒコ
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Yoshimura, Akihiko
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慶應義塾大学･医学部･教授
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Research team member
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科研費研究者番号 : 90182815
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2015
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科学研究費補助金研究成果報告書
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2014
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無菌マウスではIgE依存的な食物アレルギーへの感受性が高い。本研究の成果として, 以下のことが判明した。
①腸内細菌を持たないマウスでは腸管でgroup2 innate lymphoid cell (ILC2)の増加が見られ, 粘膜上皮細胞でInterleukin (IL)-25とIL-33の生産が亢進している。そのため, 通常のマウスに比べてアレルギー感受性が増す。②腸内細菌を持たないマウスでは粘膜でのIL-17とIL-22生産量が劇的に減少している。IL-17とIL-22がILC2からのサイトカイン生産を抑制すること, および上皮細胞からのIL-25とIL-33分泌を抑制することの2つの経路による。
Intestinal microflora has been implicated in regulation of allergies evoked by type 2 immunity. Here, we demonstrate that intestinal microflora negatively regulates murine food allergy model induced by oral ovalbumin (OVA)/cholera toxin (CT) immunization through intestinal mucosa by suppressing cytokine production from group 2 innate lymphoid cells (ILC2) cells. At early phase of OVA/CT treatment, IL-5 and 13 are mostly produced from ILC2 cells in the small intestine of immunized mice in an IL-33 dependent manner. The intestinal bacteria stimulate Th17 and γδT cell development, and IL-17 as well as IL-22 from these cells suppress food allergy, ILC2 accumulation in the intestine in vivo, and IL-5 and IL-13 expression from isolated ILC2 in vitro. Moreover, IL-33 release from the intestine was suppressed by IL-17 administration in vivo. Our results suggest that allergic diseases mediated by type 2 immunity can be prevented by the microbiota-mediated intestinal IL-23/IL-17 activation.
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研究種目 : 基盤研究(C)
研究期間 : 2011～2014
課題番号 : 23591461
研究分野 : 免疫学
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