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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adoptive Transfer, Animals, Anti-Inflammatory Agents, Antigens, CD, Cell Movement, Cells, Cultured, Coculture Techniques, Crohn Disease, Disease Models, Animal, Forkhead Transcription Factors, Gastrointestinal Agents, Immunophenotyping, Integrin alpha Chains, Intestines, Mice, Mice, Inbred BALB C, Mice, SCID, Receptors, CCR, Receptors, CCR7, Receptors, Retinoic Acid, Retinoic Acid Receptor alpha, Spleen, T-Lymphocyte Subsets, Th1 Cells, Th2 Cells, Thymus Gland, Tretinoin, Vitamin A, Vitamin A Deficiency.
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Do high and low vitamin A therapies induce distinct FoxP3+ T-cell subsets and effectively control intestinal inflammation? Context: Retinoic acid plays a positive role in induction of FoxP3(+) regulatory T cells. Because retinoic acid is produced as a metabolite of vitamin A in the intestine and FoxP3(+) T cells regulate intestinal inflammation, we investigated the impact of vitamin A status on the regulatory T cells and inflammation in the intestine. The SAMP1/YP model is a mouse model of Crohn's disease. We made vitamin A-deficient, vitamin A-excessive, and normal SAMP1/YP mice and assessed the intestinal inflammation. We also investigated the phenotype and function of FoxP3(+) T cells induced in different levels of vitamin A availability in regulation of intestinal inflammation in a T-cell-induced inflammation model in SCID mice. The limited and excessive vitamin A conditions induced distinct FoxP3(+) T-cell subsets in vivo, and both ameliorated the intestinal inflammation in SAMP1/YP mice. The limited vitamin A condition greatly induced unusual CD103(+)CCR7(+) FoxP3(+) cells, while the high vitamin A condition induced CCR9(+)alpha4beta7(+) FoxP3(+) T cells in the intestine. Both FoxP3(+) T-cell populations, when transferred into mice with ongoing intestinal inflammation, were highly effective in reversing the inflammation. Blockade or lack of occupancy of RARalpha is a mechanism to induce highly suppressive CD103(+)CCR7(+) FoxP3(+) cells in both the thymus and periphery in limited vitamin A availability.
assistant
Our results identify novel pathways of inducing highly suppressive FoxP3(+) regulatory T cells that can effectively control intestinal inflammation. The results have significant ramifications in treating inflammatory bowel diseases. Final Decision: yes