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Immune Dysfunction as a Cause and Consequence of Malnutrition

Open access
Bourke, Claire D., Berkley, James A., Prendergast, Andrew J.·2016·Trends in Immunology

Abstract

Malnutrition, which encompasses under- and overnutrition, is responsible for an enormous morbidity and mortality burden globally. Malnutrition results from disordered nutrient assimilation but is also characterized by recurrent infections and chronic inflammation, implying an underlying immune defect. Defects emerge before birth via modifications in the immunoepigenome of malnourished parents, and these may contribute to intergenerational cycles of malnutrition. This review summarizes key recent studies from experimental animals, in vitro models, and human cohorts, and proposes that immune dysfunction is both a cause and a consequence of malnutrition. Focusing on childhood undernutrition, we highlight gaps in current understanding of immune dysfunction in malnutrition, with a view to therapeutically targeting immune pathways as a novel means to reduce morbidity and mortality.

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Crossref · 10.1016/j.it.2016.04.003

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Metadata

Authors
Bourke, C. D., Berkley, J. A., & Prendergast, A. J.
Venue
Trends in Immunology
Publisher
Elsevier BV
Published
2016-06
Volume
37
Issue
6
Pages
386-398
ISSN
1471-4906 (ISSN-L)
OpenAlex
W2398393547
Cited by
725
References
18
FWCI
6.35
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Immune Dysfunction as a Cause and Consequence of Malnutrition. https://app.cochat.ai/papers/10.1016/j.it.2016.04.003
The paper
Bourke, C. D., Berkley, J. A., & Prendergast, A. J. (2016). Immune Dysfunction as a Cause and Consequence of Malnutrition. Trends in Immunology. https://doi.org/10.1016/j.it.2016.04.003

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.