Vitamin A-treated natural killer cells reduce interferon-gamma production and support regulatory T-cell differentiation
Natural killer (NK) cells are innate cytotoxic lymphocytes that contribute to immune responses against stressed, transformed, or infected cells. NK cell effector functions are regulated by microenvironmental factors, including cytokines, metabolites, and nutrients. Vitamin A is an essential micronut...
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| Main Authors: | , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
09 April 2024
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| In: |
European journal of immunology
Year: 2024, Volume: 54, Issue: 7 |
| ISSN: | 1521-4141 |
| DOI: | 10.1002/eji.202250342 |
| Online Access: | Verlag, kostenfrei, Volltext: https://doi.org/10.1002/eji.202250342 Verlag, kostenfrei, Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1002/eji.202250342 |
| Author Notes: | Mingeum Jeong, Francesco Cortopassi, Jia-Xiang See, Carolina De La Torre, Adelheid Cerwenka and Ana Stojanovic |
| Summary: | Natural killer (NK) cells are innate cytotoxic lymphocytes that contribute to immune responses against stressed, transformed, or infected cells. NK cell effector functions are regulated by microenvironmental factors, including cytokines, metabolites, and nutrients. Vitamin A is an essential micronutrient that plays an indispensable role in embryogenesis and development, but was also reported to regulate immune responses. However, the role of vitamin A in regulating NK cell functions remains poorly understood. Here, we show that the most prevalent vitamin A metabolite, all-trans retinoic acid (atRA), induces transcriptional and functional changes in NK cells leading to altered metabolism and reduced IFN-γ production in response to a wide range of stimuli. atRA-exposed NK cells display a reduced ability to support dendritic cell (DC) maturation and to eliminate immature DCs. Moreover, they support the polarization and proliferation of regulatory T cells. These results imply that in vitamin A-enriched environments, NK cells can acquire functions that might promote tolerogenic immunity and/or immunosuppression. |
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| Item Description: | Gesehen am 02.07.2024 |
| Physical Description: | Online Resource |
| ISSN: | 1521-4141 |
| DOI: | 10.1002/eji.202250342 |