| Project/Area Number |
23790528
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Immunology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
TEZUKA Hiroyuki 東京医科歯科大学, 難治疾患研究所, 助教 (30375258)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 樹状細胞 / オートファジー / 腸内常在菌 / IgA / 炎症性腸疾患 |
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| Research Abstract |
We here showed that autophagy is constitutively induced in dendritic cells (DCs) in the gut-associated lymphoid tissues (GALT) under steady-state conditions and the induction is dependent on the engulfment of commensal bacteria. In a colitis model, DC-specific autophagy-deficient mice showed a delayed restoration of mucosal integrity in a recovery phase. Autophagy-deficient GALT DCs revealed increased intracellular commensal bacteria, increased production of IL-6 and TNF-〓, and reduced production of IL-23 in the recovery phase of colitis. Importantly, the production of tissue-remodeling cytokine IL-22, which is induced by IL-23, was much reduced in the autophagy-deficient mice. Collectively, these results indicate that constitutive autophagy in GALT DCs is induced by the intracellular recognition of commensal bacteria, and suggest that the autophagy plays an important role in mucosal healing of colitis.
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