Biology and function of adipose tissue macrophages, dendritic cells and B cells

Ivanov, Stoyan; Merlin, Johanna; Lee, Man Kit Sam; Murphy, Andrew; Guinamard, Rodolphe

doi:10.1016/j.atherosclerosis.2018.01.018

Cited by 50 publications

(52 citation statements)

References 129 publications

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“…White adipose tissue (WAT) is the primary site for energy storage and a dynamic endocrine organ secreting a range of bioactive molecules (adipokines, lipokines, and extracellular vesicles) to communicate with other cell types, thereby exerting diverse local and systemic effects with a major relevance on whole‐body homeostasis . Upon exceeding its expansion capacity by an enlargement in the size of adipocytes (hypertrophy), an increase in the number of adipocytes (hyperplasia) or both, WAT becomes dysfunctional and promotes the recruitment of immune cells, which ultimately leads to a low‐grade inflammatory state . Self‐sustained lipolysis orchestrates the accumulation of monocyte‐derived macrophages in the obese WAT, where they polarize or switch from an M2 anti‐inflammatory phenotype toward an M1 pro‐inflammatory phenotype .…”

Section: Introductionmentioning

confidence: 99%

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Paz

Naranjo

López

et al. 2019

Molecular Nutrition Food Res

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Scope Obesity is a principal causative factor of metabolic syndrome. Niacin potently regulates lipid metabolism. Replacement of saturated fatty acids by MUFAs or inclusion of omega‐3 long‐chain PUFAs in the diet improves plasma lipid levels. However, the potential benefits of niacin in combination with MUFAs or omega‐3 long‐chain PUFAs against white adipose tissue (WAT) dysfunction in the high fat diet (HFD)‐induced metabolic syndrome are unknown. Methods and results Male Lepob/obLDLR−/− mice are fed a chow diet or HFDs based on milk cream (21% kcal), olive oil (21% kcal), or olive oil (20% kcal) plus 1% kcal from eicosapentaenoic and docosahexaenoic acids, including immediate‐release niacin (1% w/v) in drinking water, for 8 weeks. Mice are then phenotyped. Dietary MUFAs are identified as positive regulators of adipose NAD+ signaling pathways by triggering NAD+ biosynthesis via the salvage pathway. This coexists with overexpression of genes involved in recognition of NAD+ and fatty acids, a surrounding lipid environment dominated by exogenous oleic acid and an alternatively activated macrophage profile, which culminate in a healthy expansion of WAT and improvement of several hallmarks that typify the metabolic syndrome. Conclusion Niacin in combination with dietary MUFAs can favor WAT homeostasis in the development of HFD‐induced obesity and metabolic syndrome.

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Section: Introductionmentioning

confidence: 99%

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Paz

Naranjo

López

et al. 2019

Molecular Nutrition Food Res

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“…Innate immune responses, which constitute the body's nonspecific first line of defense against bacterial pathogens, mainly involve macrophages, dendritic cells (DCs), and natural killer (NK) cells. Innate immune cells express specific lncRNAs when the body is invaded by pathogens, and lncRNAs may thus play critical roles in regulating host–pathogen interactions and the innate immune response …”

Section: Introduction Of Lncrnasmentioning

confidence: 99%

“…DCs are antigen‐presenting cells, and their main function is to process and present antigen material on the cell surface to T cells . The lncRNA lnc‐DC is specifically expressed in human DCs, and it was identified by transcriptome chip and RNA‐Seq assays.…”

Section: Introduction Of Lncrnasmentioning

confidence: 99%

“…Innate immune cells express specific lncRNAs when the body is invaded by pathogens, and lncRNAs may thus play critical roles in regulating host-pathogen interactions and the innate immune response. 12,33,36,37 Researchers have systematically analyzed changes in lncRNA expression in macrophages upon innate immunity activation. These studies have shown that hnRNPL and linc1992 form an RNP complex that regulates transcription of tumor necrosis factor alpha (TNFα) by binding to the gene's promoter.…”

Section: Introduction Of Lncrnasmentioning

confidence: 99%

“…[40][41][42][43] DCs are antigen-presenting cells, and their main function is to process and present antigen material on the cell surface to T cells. 36 The lncRNA lnc-DC is specifically expressed in human DCs, and it was identified by transcriptome chip and RNA-Seq assays. Lnc-DC inhibits the binding of phosphatase SHP1 and STAT3, protects STAT3 Y705 phosphorylation, and enhances the STAT3 signaling pathway in DCs, consequently promoting DC maturation and activation.…”

Section: Introduction Of Lncrnasmentioning

confidence: 99%

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Long noncoding RNAs in autoimmune diseases

Lei

Jin

et al. 2018

J Biomedical Materials Res

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With the completion of the human genome project and further development of high‐throughput genomic technologies, interest in long noncoding RNAs (lncRNAs), which are defined as non‐protein‐coding RNAs at least 200 nucleotides in length, has strongly increased, and lncRNAs have become a major research direction. Increasing evidence demonstrates that lncRNAs are closely related to human growth and development and to disease occurrence via various mechanisms. lncRNAs also play crucial roles in the differentiation and activation of immune cells, and their relationships with human autoimmune diseases have received increasing attention. The development of biotechnology has led to the gradual discovery of many potential lncRNA functions. In this review, we discuss various lncRNAs that have been implicated in different human autoimmune diseases, focusing on their clinical applications as potential biomarkers and therapeutic targets in the pathologies of diverse human autoimmune diseases. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 468–475, 2019.

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Therapeutic targeting of white adipose tissue metabolic dysfunction in obesity: mechanisms and opportunities

Yang,

Chen,

Zhang

et al. 2024

MedComm

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White adipose tissue is not only a highly heterogeneous organ containing various cells, such as adipocytes, adipose stem and progenitor cells, and immune cells, but also an endocrine organ that is highly important for regulating metabolic and immune homeostasis. In individuals with obesity, dynamic cellular changes in adipose tissue result in phenotypic switching and adipose tissue dysfunction, including pathological expansion, WAT fibrosis, immune cell infiltration, endoplasmic reticulum stress, and ectopic lipid accumulation, ultimately leading to chronic low‐grade inflammation and insulin resistance. Recently, many distinct subpopulations of adipose tissue have been identified, providing new insights into the potential mechanisms of adipose dysfunction in individuals with obesity. Therefore, targeting white adipose tissue as a therapeutic agent for treating obesity and obesity‐related metabolic diseases is of great scientific interest. Here, we provide an overview of white adipose tissue remodeling in individuals with obesity including cellular changes and discuss the underlying regulatory mechanisms of white adipose tissue metabolic dysfunction. Currently, various studies have uncovered promising targets and strategies for obesity treatment. We also outline the potential therapeutic signaling pathways of targeting adipose tissue and summarize existing therapeutic strategies for antiobesity treatment including pharmacological approaches, lifestyle interventions, and novel therapies.

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Biology and function of adipose tissue macrophages, dendritic cells and B cells

Cited by 50 publications

References 129 publications

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Long noncoding RNAs in autoimmune diseases

Therapeutic targeting of white adipose tissue metabolic dysfunction in obesity: mechanisms and opportunities

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