期刊
CLINICAL & DEVELOPMENTAL IMMUNOLOGY
卷 -, 期 -, 页码 1-12出版社
HINDAWI LTD
DOI: 10.1155/2008/416910
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资金
- NIAID NIH HHS [R01 AI074745, R01AI074745, R21 AI063064, R21AI063064] Funding Source: Medline
- NIDDK NIH HHS [R01 DK076616] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI074745, R21AI063064] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK076616] Funding Source: NIH RePORTER
Vitamin A has both positive and negative regulatory functions in the immune system. While vitamin A is required for normal formation of immune cells and epithelial cell barriers, vitamin A deficiency can lead to increased inflammatory responses and tissue damage. The mechanism with which vitamin A and its metabolites such as retinoids negatively regulate inflammatory responses has not been clearly defined. Recently, it has been established that retinoids promote the generation of immune-suppressive FoxP3(+) regulatory T cells while they suppress the T cell differentiation into inflammatory Th17 cells in the periphery such as intestine. These novel functions of retinoids provide a potentially important immune regulatory mechanism. In this review, we discuss the functions of retinoids in the development of the FoxP3(+) cells and Th17 cells, the phenotype and functions of retinoid-induced FoxP3(+) T cells, and the impact of retinoid-induced FoxP3(+) T cells on the immune tolerance.
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