The source of fatty acids incorporated into proliferating lymphoid cells in immune-stimulated lymph nodes

Pond, Caroline M.; Mattacks, Christine A.

doi:10.1079/bjn2002784

Cited by 57 publications

(35 citation statements)

References 38 publications

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“…The modulation of fatty acids and glycogen within DCs influenced by IL-4, taken together with observations showing DCs in adipose tissue and the importance of perinodal triacylglycerols in the fuelling and modulation of the local immunological activities within lymph nodes, 2 has potentially wide-reaching implications. The balance amongst the type of fatty acids in perinodal fat, their effects on local cells and the cytokine interactions between DCs and the adipose tissue 52 may be fundamental in modulating local immune activity; the links amongst nutrition, metabolism and the immune system must operate at this cellular level.…”

Section: Discussionmentioning

confidence: 99%

“…The fatty acids found within the lymphocytes of lymph nodes on stimulation come largely from triacylglycerols (TAGs) in the immediately adjacent perinodal adipose tissue. 2 This perinodal fat contains more polyunsaturated fatty acids than fat remote from nodes. The perinodal type of fat, rich in n-3 fatty acids, can downregulate lymphocyte stimulation in vitro and, conversely, lymph node cells induce glycerol release from perinodal but not from other types of fat.…”

Section: Introductionmentioning

confidence: 99%

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Developing dendritic cells become ‘lacy’ cells packed with fat and glycogen

Maroof¹,

English²,

Bedford³

et al. 2005

Immunology

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SummaryOn maturation, dendritic cells (DCs) become highly active cells equipped for antigen uptake, migration and clustering and activation of T cells. We therefore asked whether DCs acquire fat and glycogen stores as they mature. DCs were generated from mouse bone marrow stem cells by culturing with granulocyte-macrophage colony-stimulating factor (GM-CSF) for 7-8 days. Stimulation of the DCs with lipopolysaccharide (LPS) for the last 24 hr of culture, or exposure to 1-15 ng/ml of interleukin (IL)-4 during development, resulted in production of DCs not only with an increased ability to stimulate T cells but also with an increasingly lacy appearance on transmission electron microscopy, with multiple unstained areas in the cytoplasm. This changed morphology was associated with the presence of increasing amounts of fat and glycogen, identified by Sudan Black and periodic acid leukofushin/Schiff (PAS) staining, respectively. Lacy DCs up-regulated type 1 and type 2 scavenger receptors, providing possible mechanisms contributing to these changes. Lacy DCs were found occasionally amongst freshly isolated splenic and lymph node DCs. DCs can be isolated from human adipose tissue, and we tested whether lacy DCs acquiring fat and glycogen were present in mouse omentum. CD45 + cells migrating from the omentum expressed specific DC markers CD11c and 33D1, costimulatory molecules and major histocompatibility complex (MHC) class II, and most showed darkly staining fat inclusions. Thus, during development, DCs can acquire large amounts of fat and glycogen, accumulation of which is promoted by antigen exposure and modulated by the cytokine milieu and location, and which may act as a link between energy stores and immune function.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Developing dendritic cells become ‘lacy’ cells packed with fat and glycogen

Maroof¹,

English²,

Bedford³

et al. 2005

Immunology

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“…The association between metabolism and inflammation is also evident in tissues of higher organisms, for example the liver and adipose tissue, where immune effector cells, such as Kupffer cells and macrophages, are found alongside hepatocytes and adipocytes, respectively1. Interestingly, lymph nodes are also embedded in adipose tissue, perhaps to have a competitive advantage over other tissues in meeting excessive energy demands at times of immune stress10. In addition, the perinodal adipose tissue, which is located around the lymph nodes, might influence local immune responses owing to its high polyunsaturated fatty-acid content, which could provide nutrients and soluble mediators that are needed for the responses, and the presence of dendritic cells11.…”

mentioning

confidence: 99%

Nutrient sensing and inflammation in metabolic diseases

2008

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The proper functioning of the pathways that are involved in the sensing and management of nutrients is central to metabolic homeostasis and is therefore among the most fundamental requirements for survival. Metabolic systems are integrated with pathogen-sensing and immune responses, and these pathways are evolutionarily conserved. This close functional and molecular integration of the immune and metabolic systems is emerging as a crucial homeostatic mechanism, the dysfunction of which underlies many chronic metabolic diseases, including type 2 diabetes and atherosclerosis. In this Review we provide an overview of several important networks that sense and manage nutrients and discuss how they integrate with immune and inflammatory pathways to influence the physiological and pathological metabolic states in the body.The integration of metabolism and immunity (or of nutrient-and pathogen-sensing pathways) can be traced back to an evolutionary need for survival, which resulted in the co-development of the organ systems and signalling pathways that mediate these two processes 1 . The pressure to survive would have favoured energy efficiency and storage to prepare for times of food deprivation and for mounting a potent immune response to defend the host against infectious agents. However, the initiation and maintenance of immunity is a metabolically costly endeavour and cannot operate efficiently under conditions of energy deficit 2,3 . For example, fever is associated with a 7-13% increase in caloric energy consumption per 1°C increase in body temperature, the energy expenditure of which is estimated to equate to 9.4×10 6 joules; this is approximately the energy cost of a 70 kg person walking 45 km 4,5 . Sepsis can increase the human metabolic rate by 30-60% 6 . Furthermore, the production and maintenance of phagocytes during infection is thought to result in an energy consumption of approximately 7.9×10 5 joules 4 .It is also clear that starvation and malnutrition can impair immune function; a total reduction in body fat has been shown to result in a decrease in the energy that is available for immune responses in rodents 7 . In addition, conditions that trigger an immune response during starvation can severely reduce the survival of insects 8 . Therefore, immune defence is subject to a tradeoff between other energy-demanding processes, such as reproduction, thermoregulation and lactation. Interestingly, energy surplus (which is typical of individuals who are obese or suffer from metabolic syndrome) can also impair immune responses and induce chronic inflammation (see later). Therefore, a balanced energy flux and maintainance of favourable metabolic homeostasis are required for the proper functioning of the immune system. These processes may have been optimized through the close coordination and co-evolution of metabolic and immune responses, and of the organs that are involved in these processes.Correspondence to G.S.H. ghotamis@hsph.harvard.edu. Competing interests statementThe author(s) declare(s) competi...

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“…Perinodal adipocytes are instead stimulated to undergo lipolysis with cytokines, such as TNFα and IL-6, that are released by local immune cells [48, 49]. Most of the lipids in new lymphoid cells are derived from triacylglycerols in perinodal adipocytes [50]. Perinodal adipocytes fuel the local immune response, as needed, without depending on circulating energy reserves.…”

Section: Mat and Hematopoiesismentioning

confidence: 99%

Evolution of the Marrow Adipose Tissue Microenvironment

Craft

Scheller

2016

Calcif Tissue Int

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Adipocytes of the marrow adipose tissue (MAT) are distributed throughout the skeleton, are embedded in extracellular matrix, and are surrounded by cells of the hematopoietic and osteogenic lineages. MAT is a persistent component of the skeletal microenvironment and has the potential to impact local processes including bone accrual and hematopoietic function. In this review, we discuss the initial evolution of MAT in vertebrate lineages while emphasizing comparisons to the development of peripheral adipose, hematopoietic, and skeletal tissues. We then apply these evolutionary clues to define putative functions of MAT. Lastly, we explore the regulation of MAT by two major components of its microenvironment, the extracellular matrix and the nerves embedded within. The extracellular matrix and nerves contribute to both rapid and continuous modification of the MAT niche and may help to explain evolutionary conserved mechanisms underlying the coordinated regulation of blood, bone, and MAT within the skeleton.

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The source of fatty acids incorporated into proliferating lymphoid cells in immune-stimulated lymph nodes

Cited by 57 publications

References 38 publications

Developing dendritic cells become ‘lacy’ cells packed with fat and glycogen

Developing dendritic cells become ‘lacy’ cells packed with fat and glycogen

Nutrient sensing and inflammation in metabolic diseases

Evolution of the Marrow Adipose Tissue Microenvironment

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