Reprogramming of the immune system during zinc deficiency
Abstract
Thymic atrophy, lymphopenia, and compromised cell- and antibody-mediated responses that cause increased rates of infections of longer duration are the immunological hallmarks of zinc deficiency (ZD) in humans and higher animals. As the deficiency advances, a reprogramming of the immune system occurs, beginning with the activation of the stress axis and chronic production of glucocorticoids that accelerate apoptosis among pre-B and -T cells. This reduces lymphopoiesis and causes atrophy of the thymus. In contrast, myelopoiesis is preserved, thereby providing protection for the first line of immune defense or innate immunity. Changes in gene expression for cytokines, DNA repair enzymes, zinc transporters, signaling molecules, etc., suggest that cells of the immune system are attempting to adapt to the stress of suboptimal zinc. Better understanding of the molecular and cellular changes made in response to inadequate zinc should lead to the development of immunotherapeutic interventions.
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Zinc deficiency can cause decreased levels of serum thymulin, a zinc-dependent peptide hormone produced by thymic epithelial cells, whose activity is progressively reduced with age and peaks in pre-adolescence.
“Zinc deficiency can cause decreased levels of serum thymulin, a zinc dependent peptide hormone produced by thymic epithelial cells, with an activity that is progressively reduced with age, with a peak in pre-adolescence (78, 104, 108).”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [108]
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“, 1999), reduced lymphocyte proliferation, and reduced levels of circulating T lymphocytes, CD4 memory T cells, and naive T cells (Barnett et al., 2010; Fraker and King, 2004).”
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- Authors
- Fraker, P. J., & King, L. E.
- Affiliations
- Michigan State University (US)
- Venue
- Annual Review of Nutrition
- Publisher
- Annual Reviews
- Published
- 2004-07-14
- Volume
- 24
- Issue
- 1
- Pages
- 277-298
- ISSN
- 0199-9885 (ISSN-L)
- 1545-4312
- OpenAlex
- W2102050228
- Cited by
- 470
- References
- 66
- Citations by year
- 2026: 4 · 2025: 19 · 2024: 12 · 2023: 17 · 2022: 18 · 2021: 31 · 2020: 21 · 2019: 21 · 2018: 22 · 2017: 29 · 2016: 22 · 2015: 32 · 2014: 40 · 2013: 24 · 2012: 32
- FWCI
- 1.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-55, 289-25)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
- Keywords
- zinc deficiency, immune reprogramming, thymic atrophy, lymphopenia, glucocorticoids, stress axis, apoptosis, lymphocyte development, myelopoiesis, innate immunity, cytokine gene expression, DNA repair enzymes, zinc transporters, infection susceptibility
- MeSH terms
- Antibody Formation, Erythropoiesis, Gene Expression Regulation, Glucocorticoids, Humans, Immune System, Immunity, Cellular, Zinc, Apoptosis, Myelopoiesis
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