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Iron-dependent histone 3 lysine 9 demethylation controls B cell proliferation and humoral immune responses
Open accessAbstract
Trace elements play important roles in human health, but little is known about their functions in humoral immunity. Here, we show an important role for iron in inducing cyclin E and B cell proliferation. We find that iron-deficient individuals exhibit a significantly reduced antibody response to the measles vaccine when compared to iron-normal controls. Mice with iron deficiency also exhibit attenuated T-dependent or T-independent antigen-specific antibody responses. We show that iron is essential for B cell proliferation; both iron deficiency and α-ketoglutarate inhibition could suppress cyclin E1 induction and S phase entry of B cells upon activation. Finally, we demonstrate that three demethylases, KDM2B, KDM3B and KDM4C, are responsible for histone 3 lysine 9 (H3K9) demethylation at the cyclin E1 promoter, cyclin E1 induction and B cell proliferation. Thus, our data reveal a crucial role of H3K9 demethylation in B cell proliferation, and the importance of iron in humoral immunity.
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Human patients with iron deficiency show significantly weakened antibody responses when challenged with the measles vaccine.
“Intriguingly, human patients with iron deficiency also show significantly weakened antibody responses when challenged with the measles vaccine.”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Jiang et al., 2019
Iron deficiency in mice led to dramatically attenuated antigen-specific antibody responses.
“Iron deficiency in mice led to dramatically attenuated antigen-specific antibody responses (Jiang et al., 2019).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Jiang et al., 2019
A link between intracellular iron levels and epigenetic programming has been described to control B cell activation, proliferation and antibody responses at the level of H3K9 demethylation at the promoter region of the cell-cycle regulator cyclin E1.
“Interestingly a link between intracellular iron levels and epigenetic programming has also been described to control B cell activation, proliferation and antibody responses at the level of H3K9 demethylation at the promoter region of the cell-cycle regulator, cyclin E1 (Jiang et al., 2019).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Jiang et al., 2019
Iron-deficient mice have massively attenuated T-cell-dependent and T-cell-independent antigen-specific antibody responses.
“Accordingly iron deficient mice led to massively attenuated T-cell-dependent and T-cell-independent antigen-specific antibody responses and human patients with iron deficiency presented significantly weakened antibody response to measles vaccine [128].”
From Iron in immune cell function and host defense (2021) · cites this paper as [128]
Human patients with iron deficiency have a significantly weakened antibody response to measles vaccine.
“Accordingly iron deficient mice led to massively attenuated T-cell-dependent and T-cell-independent antigen-specific antibody responses and human patients with iron deficiency presented significantly weakened antibody response to measles vaccine [128].”
From Iron in immune cell function and host defense (2021) · cites this paper as [128]
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References 40 · Cited by 208
Metadata
- Authors
- Jiang, Y., Li, C., Wu, Q., An, P., Huang, L., Wang, J., Chen, C., Chen, X., Zhang, F., Ma, L., Liu, S., He, H., Xie, S., Sun, Y., Liu, H., Zhan, Y., Tao, Y., Liu, Z., Sun, X., Hu, Y., Wang, Q., Ye, D., Zhang, J., Zou, S., Wang, Y., Wei, G., Liu, Y., Shi, Y., Eugene Chin, Y., Hao, Y., Wang, F., & Zhang, X.
- Affiliations
- Shanghai Institute of Nutrition and Health (CN)
- Zhengzhou University (CN)
- Fudan University (CN)
- Chinese Academy of Sciences (CN)
- Zhejiang Center for Disease Control and Prevention (CN)
- Shanghai Jiao Tong University (CN)
- Corresponding author
- Wang, Fudi
- Zhang, Xiaoren
- ORCID
- Venue
- Nature Communications
- Published
- 2019-07-03
- Volume
- 10
- Issue
- 1
- Pages
- 2935-2935
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC6610088
- OpenAlex
- W2955390397
- Cited by
- 208
- References
- 40
- Citations by year
- 2026: 26 · 2025: 25 · 2024: 37 · 2023: 23 · 2022: 36 · 2021: 44 · 2020: 16 · 2019: 1
- FWCI
- 10.07
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Natural Science Foundation of China (31530034, 31570902, 31370881)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Keywords
- iron deficiency, B cell proliferation, humoral immunity, cyclin E1, KDM2B, KDM3B, KDM4C, alpha-ketoglutarate, T cell-dependent antibody response, T-independent antibody response, S phase entry, trace elements
- MeSH terms
- Demethylation, Animals, B-Lymphocytes, Cell Cycle, Cells, Cultured, Histones, Iron, Lymphocyte Activation, Lysine, Mice, Inbred C57BL, Promoter Regions, Genetic, T-Lymphocytes, Oncogene Proteins, Cyclin E, F-Box Proteins, Cell Proliferation, Mice, Jumonji Domain-Containing Histone Demethylases, Immunity, Humoral
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