Leptin levels in patients with systemic lupus erythematosus inversely correlate with regulatory T cell frequency

X, Wang; Qiao, Yu; Li, Yang; Song, Seung Hwan; Han, Yuxiang; Tian, Yu; Ding, Meng; Jin, Hongtao; Shao, Fang; Liu, A

doi:10.1177/0961203317703497

Cited by 39 publications

(28 citation statements)

References 26 publications

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“…Accordingly, Lepr -deficient rats developed less severe hypoxia-induced pulmonary hypertension and were protected against decreased Treg function after exposure to hypoxia ( Huertas et al, 2016 ). In SLE, the disease-associated higher leptin serum levels were negatively correlated with disease severity and number of Treg cells ( Ma et al, 2015 ; Margiotta et al, 2016 ; Wang et al, 2017 ), and fasting-induced hypoleptinaemia was related to Treg population recovery in lupus-prone mice ( Liu et al, 2012 ). Leptin-deficient ob/ob mice and a mouse model of lupus with leptin deficiency demonstrated increased frequency of Tregs cells ( Fujita et al, 2014 ; Lourenço et al, 2016 ).…”

Section: Leptin and Adaptive Immunity ( Figure mentioning

confidence: 99%

Obesity, Fat Mass and Immune System: Role for Leptin

et al. 2018

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Obesity is an epidemic disease characterized by chronic low-grade inflammation associated with a dysfunctional fat mass. Adipose tissue is now considered an extremely active endocrine organ that secretes cytokine-like hormones, called adipokines, either pro- or anti-inflammatory factors bridging metabolism to the immune system. Leptin is historically one of most relevant adipokines, with important physiological roles in the central control of energy metabolism and in the regulation of metabolism-immune system interplay, being a cornerstone of the emerging field of immunometabolism. Indeed, leptin receptor is expressed throughout the immune system and leptin has been shown to regulate both innate and adaptive immune responses. This review discusses the latest data regarding the role of leptin as a mediator of immune system and metabolism, with particular emphasis on its effects on obesity-associated metabolic disorders and autoimmune and/or inflammatory rheumatic diseases.

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Section: Leptin and Adaptive Immunity ( Figure mentioning

confidence: 99%

Obesity, Fat Mass and Immune System: Role for Leptin

et al. 2018

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“…Leptin signaling has also been implicated in several other autoimmune diseases. In systemic lupus erythematosus (SLE), leptin levels have been reported to be elevated in human patients and correlate with severity in a mouse model of the disease ( 134 , 135 ). Decreasing leptin signaling through genetic knockout or antibody blockade protected against disease and increased Treg cell numbers in SLE mice ( 134 ).…”

Section: Effect Of Nutritional Status On Immune-mediated Diseasementioning

confidence: 99%

Changes in Nutritional Status Impact Immune Cell Metabolism and Function

Alwarawrah¹,

Kiernan²,

MacIver³

2018

Front. Immunol.

377

254

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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.

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“…97 Leptin levels inversely correlate with the frequency of Treg cells in SLE patients. 83 Leptin deficiency in MRL/lpr lupus-prone mice was protective for disease development, and it increased the frequency of Treg cells. 98 Likewise, leptin inhibited Treg cell polarization in vitro and its neutralization resulted in Treg cell expansion in NZB/W mice.…”

Section: Lupus and Sys Temi C Me Tabolis Mmentioning

confidence: 98%

“…81 High levels of circulating leptin correlate with disease activity in SLE patients. 63,[82][83][84][85][86] Fasting decreases the production of leptin and expands the frequency of FOXP3 + regulatory (Treg) cells in SLE patients leading to a reduced disease activity. 87 However, SLE patients with reduced serum leptin have also been reported in some studies, 88,89 while others show no difference between SLE patients and HCs.…”

Section: Lupus and Sys Temi C Me Tabolis Mmentioning

confidence: 99%

Metabolic determinants of lupus pathogenesis

Teng

Brown

Choi

et al. 2020

Immunological Reviews

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The metabolism of healthy murine and more recently human immune cells has been investigated with an increasing amount of details. These studies have revealed the challenges presented by immune cells to respond rapidly to a wide variety of triggers by adjusting the amount, type, and utilization of the nutrients they import. A concept has emerged that cellular metabolic programs regulate the size of the immune response and the plasticity of its effector functions. This has generated a lot of enthusiasm with the prediction that cellular metabolism could be manipulated to either enhance or limit an immune response. In support of this hypothesis, studies in animal models as well as human subjects have shown that the dysregulation of the immune system in autoimmune diseases is associated with a skewing of the immunometabolic programs. These studies have been mostly conducted on autoimmune CD4 + T cells, with the metabolism of other immune cells in autoimmune settings still being understudied. Here we discuss systemic metabolism as well as cellular immunometabolism as novel tools to decipher fundamental mechanisms of autoimmunity. We review the contribution of each major metabolic pathway to autoimmune diseases, with a focus on systemic lupus erythematosus (SLE), with the relevant translational opportunities, existing or predicted from results obtained with healthy immune cells. Finally, we review how targeting metabolic programs may present novel therapeutic venues. K E Y W O R D Sglucose, glutamine, lupus, metabolic inhibitors, metabolism

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Leptin levels in patients with systemic lupus erythematosus inversely correlate with regulatory T cell frequency

Cited by 39 publications

References 26 publications

Obesity, Fat Mass and Immune System: Role for Leptin

Obesity, Fat Mass and Immune System: Role for Leptin

Changes in Nutritional Status Impact Immune Cell Metabolism and Function

Metabolic determinants of lupus pathogenesis

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