Vitamin A Deficiency Impairs Induction of Oral Tolerance in Mice

• Published in: Journal of Nutritional Science and Vitaminology Vol. 61; no. 2; pp. 147 - 153
• Main Authors: NAKAMOTO, Akiko, SHUTO, Emi, TSUTSUMI, Rie, NAKAMOTO, Mariko, NII, Yoshitaka, SAKAI, Tohru
• Format: Journal Article
• Language: English
• Published: Japan Center for Academic Publications Japan 2015
• Subjects: Administration, Oral; Animals; Antibodies - metabolism; antibody; CD11 Antigens; CD11c+ cells; CD4 Antigens; Cytokines - biosynthesis; Forkhead Transcription Factors - metabolism; Immune Tolerance; Immunity, Active; Lymph Nodes; Mice, Inbred BALB C; oral tolerance; Ovalbumin - immunology; regulatory T cells; T-Lymphocytes, Regulatory - metabolism; Vitamin A - metabolism; vitamin A deficiency; Vitamin A Deficiency - complications; Vitamin A Deficiency - metabolism
• ISSN: 0301-4800; 1881-7742
• 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.