The DOI matches its Crossref record; 250 of the 250 references it cites were found in a registry or an index.
Zinc and immune function: the biological basis of altered resistance to infection
Open accessAbstract
Zinc is known to play a central role in the immune system, and zinc-deficient persons experience increased susceptibility to a variety of pathogens. The immunologic mechanisms whereby zinc modulates increased susceptibility to infection have been studied for several decades. It is clear that zinc affects multiple aspects of the immune system, from the barrier of the skin to gene regulation within lymphocytes. Zinc is crucial for normal development and function of cells mediating nonspecific immunity such as neutrophils and natural killer cells. Zinc deficiency also affects development of acquired immunity by preventing both the outgrowth and certain functions of T lymphocytes such as activation, Th1 cytokine production, and B lymphocyte help. Likewise, B lymphocyte development and antibody production, particularly immunoglobulin G, is compromised. The macrophage, a pivotal cell in many immunologic functions, is adversely affected by zinc deficiency, which can dysregulate intracellular killing, cytokine production, and phagocytosis. The effects of zinc on these key immunologic mediators is rooted in the myriad roles for zinc in basic cellular functions such as DNA replication, RNA transcription, cell division, and cell activation. Apoptosis is potentiated by zinc deficiency. Zinc also functions as an antioxidant and can stabilize membranes. This review explores these aspects of zinc biology of the immune system and attempts to provide a biological basis for the altered host resistance to infections observed during zinc deficiency and supplementation.
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In the citing paper
“Both human and animal studies have shown a correlation between zinc deficiency and enhanced susceptibility to infection.”
From Metal ion acquisition in Staphylococcus aureus: overcoming nutritional immunity (2012) · cites this paper as [190]
In the citing paper
“Many animal studies show that zinc deficiency decreases resistance to a range of bacterial, viral, fungal, and parasitic pathogens (29), probably because of the immune impairment induced by zinc deficiency.”
From Zinc supplementation decreases incidence of infections in the elderly: effect of zinc on generation of cytokines and oxidative stress (2007) · cites this paper as [29]
In the citing paper
“Many animal studies show that zinc deficiency decreases resistance to a range of bacterial, viral, fungal, and parasitic pathogens (29), probably because of the immune impairment induced by zinc deficiency.”
From Zinc supplementation decreases incidence of infections in the elderly: effect of zinc on generation of cytokines and oxidative stress (2007) · cites this paper as [29]
In the citing paper
“Zinc supplementation decreased not only the production of inflammatory cytokines but also that of oxidative stress markers, as we previously reported (19,29).”
From Zinc supplementation decreases incidence of infections in the elderly: effect of zinc on generation of cytokines and oxidative stress (2007) · cites this paper as [29]
In the citing paper
“Numerous studies have shown the benefits of zinc supplementation with respect to infectious diseases in human populations (29).”
From Zinc supplementation decreases incidence of infections in the elderly: effect of zinc on generation of cytokines and oxidative stress (2007) · cites this paper as [29]
In the citing paper
“Zinc supplementation decreased not only the production of inflammatory cytokines but also that of oxidative stress markers, as we previously reported (19,29).”
From Zinc supplementation decreases incidence of infections in the elderly: effect of zinc on generation of cytokines and oxidative stress (2007) · cites this paper as [29]
In the citing paper
“Zinc deficiency affects T helper subset 1 cell function adversely in humans (36–38, 43).”
From Discovery of Human Zinc Deficiency: Its Impact on Human Health and Disease (2013) · cites this paper as [43]
In the citing paper
“The intracellular zinc concentration, such as the lymphocyte zinc concentration, is a better indicator of zinc status as we previously reported (4,6).”
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Self-citation
Metadata
- Authors
- Shankar, A. H., & Prasad, A. S.
- Affiliations
- Johns Hopkins University (US)
- Venue
- The American Journal of Clinical Nutrition
- Publisher
- Elsevier BV
- Published
- 1998-08
- Volume
- 68
- Issue
- 2
- Pages
- 447S-463S
- ISSN
- 0002-9165 (ISSN-L)
- OpenAlex
- W1943607432
- Cited by
- 1,606
- References
- 250
- Citations by year
- 2026: 33 · 2025: 53 · 2024: 46 · 2023: 52 · 2022: 70 · 2021: 90 · 2020: 98 · 2019: 65 · 2018: 52 · 2017: 77 · 2016: 84 · 2015: 61 · 2014: 91 · 2013: 70 · 2012: 68
- FWCI
- 8.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal of Clinical Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Johns Hopkins University (HRN-A-00-97-00015-00)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Plant Micronutrient Interactions and Effects
- Keywords
- zinc, zinc deficiency, immune function, infection susceptibility, non-specific immunity, natural killer cells, neutrophils, T cell activation, Th1 cytokines, B cells, antibody production, IgG, macrophages, phagocytosis, apoptosis, antioxidant function, zinc supplementation
- MeSH terms
- Animals, Glucocorticoids, Humans, Immunity, Infections, Thymic Factor, Circulating, Zinc, Cytokines, Apoptosis
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