Abstract
The vitamin A metabolites, including retinoic acid (RA), form ligands for retinoic acid-related nuclear receptors and together they play pleiotropic roles in various biological processes. Recently, we described that RA also functions as a key modulator of transforming growth factor-beta (TGF-beta)-driven immune deviation, capable of suppressing the differentiation of interleukin-17 secreting T helper cells (T(H)17) and conversely promoting the generation of Foxp3(+) T regulatory (Treg) cells. This review will focus on the role of RA in the reciprocal TGF-beta-driven differentiation of T(H)17 and Treg and on the importance of such regulatory mechanism to control a functional immune system, in particular at the mucosal interface of the intestine.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Aldehyde Dehydrogenase / immunology
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Aldehyde Dehydrogenase / metabolism
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Animals
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Antineoplastic Agents / immunology
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Antineoplastic Agents / metabolism
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Cell Nucleus / immunology
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Cell Nucleus / metabolism
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Diet
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Forkhead Transcription Factors / immunology
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Forkhead Transcription Factors / metabolism
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Humans
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Interleukin-17 / immunology
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Interleukin-17 / metabolism
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Intestinal Mucosa / immunology*
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Intestinal Mucosa / metabolism
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Receptors, Retinoic Acid / immunology
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Receptors, Retinoic Acid / metabolism
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T-Lymphocytes, Helper-Inducer / immunology*
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T-Lymphocytes, Helper-Inducer / metabolism
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Transforming Growth Factor beta / immunology
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Transforming Growth Factor beta / metabolism*
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Tretinoin / immunology
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Tretinoin / metabolism*
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Vitamin A / immunology
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Vitamin A / metabolism*
Substances
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Antineoplastic Agents
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Forkhead Transcription Factors
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Interleukin-17
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Receptors, Retinoic Acid
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Transforming Growth Factor beta
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Vitamin A
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Tretinoin
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Aldehyde Dehydrogenase