Vitamin A and retinoic acid in T cell-related immunity
Open accessAbstract
Interest in vitamin A as a regulator of immune function goes back to the early 1900s. Recently, several lines of evidence have converged to show that retinoic acid (RA), a major oxidative metabolite of vitamin A, plays a key role in the differentiation of T cell subsets, the migration of T cells into tissues, and the proper development of T cell-dependent antibody responses. This review discusses evidence from experimental studies that RA promotes the differentiation of regulatory T cells, which help to suppress inflammatory reactions, and plays a significant role in normal mucosal immunity by modulating T cell activation and regulating cell trafficking. RA also promotes antibody responses to T cell-dependent antigens. Conversely, in a state of vitamin A deficiency, inflammatory T cell reactions may be inadequately opposed and therefore become dominant. Although data from human studies are still needed, the framework now developed from studies in mice and rat models suggests that adequate vitamin A status, whether derived from ingestion of preformed retinol or β-carotene, is important for maintaining a proper balance of well-regulated T cell functions and for preventing excessive or prolonged inflammatory reactions.
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In the presence of vitamin A, IL-2 levels are increased, which stimulates differentiation of T cells into regulatory T cells.
“In the presence of vitamin A, IL-2 levels are increased, which stimulates the differentiation of T cells into regulatory T cells, which are important mediators for the prevention of autoimmune responses [129,208].”
From Vitamin A Update: Forms, Sources, Kinetics, Detection, Function, Deficiency, Therapeutic Use and Toxicity (2021) · cites this paper as [208]
The section “RA in the Regulation of T Cell Differentiation” (pp. 1–4) says retinoic acid favors induced regulatory T-cell differentiation when TGF-β is present and IL-6 is low. It does not say vitamin A increases IL-2 levels or that increased IL-2 drives this differentiation. (LLM, conf=0.88)
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- Authors
- Ross, A. C.
- Affiliations
- Pennsylvania State University (US)
- Corresponding author
- Ross, A Catharine
- ORCID
- Ross, A Catharine
- Venue
- The American Journal of Clinical Nutrition
- Publisher
- Elsevier BV
- Published
- 2012-11
- Volume
- 96
- Issue
- 5
- Pages
- 1166S-1172S
- ISSN
- 0002-9165 (ISSN-L)
- PMC
- PMC3471201
- OpenAlex
- W2170235819
- Cited by
- 261
- References
- 75
- Citations by year
- 2026: 18 · 2025: 32 · 2024: 12 · 2023: 13 · 2022: 14 · 2021: 19 · 2020: 23 · 2019: 21 · 2018: 16 · 2017: 19 · 2016: 18 · 2015: 20 · 2014: 23 · 2013: 9 · 2012: 2
- FWCI
- 1.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal of Clinical Nutrition (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (DK-41479)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK041479, R56DK041479, DK41479)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD066982, R01HD066982)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- vitamin A, retinoic acid, T cell immunity, regulatory T cells, T cell differentiation, T cell migration, mucosal immunity, T cell-dependent antibody response, vitamin A deficiency, inflammation, retinol, beta-carotene, T cell activation
- MeSH terms
- Animals, B-Lymphocytes, Cell Differentiation, Humans, Intestines, Tretinoin, Vitamin A, T-Lymphocyte Subsets, Immunity, Mucosal, T-Lymphocytes, Regulatory
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