Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 May 16:9:1055.
doi: 10.3389/fimmu.2018.01055. eCollection 2018.

Changes in Nutritional Status Impact Immune Cell Metabolism and Function

Yazan Alwarawrah  1 , Kaitlin Kiernan  2 , Nancie J MacIver  1   2   3
Affiliations
Review

Changes in Nutritional Status Impact Immune Cell Metabolism and Function

Yazan Alwarawrah et al. Front Immunol. .

Abstract

Immune cell function and metabolism are closely linked. Many studies have now clearly demonstrated that alterations in cellular metabolism influence immune cell function and that, conversely, immune cell function determines the cellular metabolic state. Less well understood, however, are the effects of systemic metabolism or whole organism nutritional status on immune cell function and metabolism. Several studies have demonstrated that undernutrition is associated with immunosuppression, which leads to both increased susceptibility to infection and protection against several types of autoimmune disease, whereas overnutrition is associated with low-grade, chronic inflammation that increases the risk of metabolic and cardiovascular disease, promotes autoreactivity, and disrupts protective immunity. Here, we review the effects of nutritional status on immunity and highlight the effects of nutrition on circulating cytokines and immune cell populations in both human studies and mouse models. As T cells are critical members of the immune system, which direct overall immune response, we will focus this review on the influence of systemic nutritional status on T cell metabolism and function. Several cytokines and hormones have been identified which mediate the effects of nutrition on T cell metabolism and function through the expression and action of key regulatory signaling proteins. Understanding how T cells are sensitive to both inadequate and overabundant nutrients may enhance our ability to target immune cell metabolism and alter immunity in both malnutrition and obesity.

Keywords: T cells; cellular metabolism; inflammation; leptin; malnutrition; obesity.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Suggested links between nutritional status, immune metabolism, and immune function. In settings of extreme nutritional status (obesity or malnutrition), changes in immune cell populations, hormones, and cytokine levels lead to alternations in immune cell metabolism, which thereby influence immune function.
See this image and copyright information in PMC

References

    1. Hotamisligil GS, Shargill NS, Spiegelman BM. Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Science (1993) 259(5091):87–91.10.1126/science.7678183 - DOI - PubMed
    1. Hotamisligil GS, Arner P, Caro JF, Atkinson RL, Spiegelman BM. Increased adipose tissue expression of tumor necrosis factor-alpha in human obesity and insulin resistance. J Clin Invest (1995) 95(5):2409–15.10.1172/JCI117936 - DOI - PMC - PubMed
    1. Kern PA, Saghizadeh M, Ong JM, Bosch RJ, Deem R, Simsolo RB. The expression of tumor necrosis factor in human adipose tissue. Regulation by obesity, weight loss, and relationship to lipoprotein lipase. J Clin Invest (1995) 95(5):2111–9.10.1172/JCI117899 - DOI - PMC - PubMed
    1. Uysal KT, Wiesbrock SM, Marino MW, Hotamisligil GS. Protection from obesity-induced insulin resistance in mice lacking TNF-alpha function. Nature (1997) 389(6651):610–4.10.1038/39335 - DOI - PubMed
    1. Sewter CP, Digby JE, Blows F, Prins J, O’Rahilly S. Regulation of tumour necrosis factor-alpha release from human adipose tissue in vitro. J Endocrinol (1999) 163(1):33–8.10.1677/joe.0.1630033 - DOI - PubMed

Publication types