Nakamoto Akiko, Shuto Emi, Tsutsumi Rie, Nakamoto Mariko, Nii Yoshitaka, Sakai Tohru
Department of Public Health and Applied Nutrition, Institution of Health Bioscience, The University of Tokushima Graduate School.
J Nutr Sci Vitaminol (Tokyo). 2015;61(2):147-53. doi: 10.3177/jnsv.61.147.
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.
口服耐受是一种对经口服摄入的抗原产生全身性无反应性以及免疫应答丧失的诱导现象。研究表明维生素A在体外口服耐受中具有重要作用，但在体内实验模型中并非如此。因此，我们开展了实验以确定维生素A缺乏如何影响耐受诱导以及肠系膜淋巴结（MLN）CD11c(+)细胞诱导调节性T细胞（Tregs）的能力。在维生素A充足的小鼠中，通过口服卵清蛋白（OVA）诱导免疫耐受。OVA特异性抗体和细胞因子的产生显著减少。另一方面，在维生素A缺乏的小鼠中，口服OVA并未抑制OVA特异性抗体和细胞因子的产生。关于Tregs的诱导，在维生素A缺乏的小鼠中，CD11c(+)细胞使初始CD4(+)细胞转化为Foxp3(+)细胞的转化率降低。我们的研究表明，维生素A缺乏会导致体内口服耐受的破坏。
