Vitamin A Deficiency Impairs Induction of Oral Tolerance in Mice
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- NAKAMOTO Akiko
- Department of Public Health and Applied Nutrition, Institution of Health Bioscience, The University of Tokushima Graduate School
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- SHUTO Emi
- Department of Public Health and Applied Nutrition, Institution of Health Bioscience, The University of Tokushima Graduate School
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- TSUTSUMI Rie
- Department of Public Health and Applied Nutrition, Institution of Health Bioscience, The University of Tokushima Graduate School
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- NAKAMOTO Mariko
- Department of Public Health and Applied Nutrition, Institution of Health Bioscience, The University of Tokushima Graduate School
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- NII Yoshitaka
- Food and Biotechnology Division, Tokushima Prefectural Industrial Technology Center
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- SAKAI Tohru
- Department of Public Health and Applied Nutrition, Institution of Health Bioscience, The University of Tokushima Graduate School
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抄録
Oral tolerance is a phenomenon of induction of systemic unresponsiveness to antigens ingested by the oral route and loss of immune response. Studies have shown the importance of vitamin A in oral tolerance in vitro but not in an in vivo experimental model. Therefore, we carried out experiments to determine how vitamin A deficiency affects tolerance induction and the ability of mesenteric lymph node (MLN) CD11c+ cells to induce regulatory T cells (Tregs). Immunological tolerance was induced by oral ovalbumin (OVA) administration in vitamin A-sufficient mice. OVA-specific antibody and cytokine production were significantly reduced. On the other hand, in vitamin A-deficient mice, both OVA-specific antibody and cytokine production were not suppressed by oral OVA administration. Regarding induction of Tregs, the conversion rate of Foxp3+ cells from naïve CD4+ cell by CD11c+ cells was decreased in vitamin A-deficient mice. Our study indicates that vitamin A deficiency causes the breakdown of oral tolerance in vivo.
収録刊行物
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- Journal of Nutritional Science and Vitaminology
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Journal of Nutritional Science and Vitaminology 61 (2), 147-153, 2015
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詳細情報 詳細情報について
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- CRID
- 1390001206323984000
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- NII論文ID
- 130005074125
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- NII書誌ID
- AA00703822
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- ISSN
- 18817742
- 03014800
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- NDL書誌ID
- 026378882
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- PubMed
- 26052145
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- 抄録ライセンスフラグ
- 使用不可