Immune cell metabolism in autoimmunity

Teng, Xiangyu; Li, W; Cornaby, Caleb; Morel, Laurence

doi:10.1111/cei.13277

Cited by 27 publications

(16 citation statements)

References 128 publications

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“…Aerobic glycolysis is a central requirement for meeting the bioenergetic and biosynthetic needs of rapidly proliferating cancer cells. [5][6][7] This metabolic change of cancer cells may not only have an impact on immune cells but also the immune cells themselves can cause metabolic reprogramming to drive their activation and differentiation in response to pathogen-derived or inflammatory signals, thereby supporting distinct immune effector functions. 5,8 Indeed, each subset of immune cells has distinct metabolic requirements at different stages of differentiation.…”

Section: Introductionmentioning

confidence: 99%

Energy metabolism manipulates the fate and function of tumour myeloid-derived suppressor cells

Pang

Lin

et al. 2019

Br J Cancer

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In recent years, a large number of studies have been carried out in the field of immune metabolism, highlighting the role of metabolic energy reprogramming in altering the function of immune cells. Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of cells generated during a large array of pathological conditions, such as cancer, inflammation, and infection, and show remarkable ability to suppress T-cell responses. These cells can also change their metabolic pathways in response to various pathogen-derived or inflammatory signals. In this review, we focus on the roles of glucose, fatty acid (FA), and amino acid (AA) metabolism in the differentiation and function of MDSCs in the tumour microenvironment, highlighting their potential as targets to inhibit tumour growth and enhance tumour immune surveillance by the host. We further highlight the remaining gaps in knowledge concerning the mechanisms determining the plasticity of MDSCs in different environments and their specific responses in the tumour environment. Therefore, this review should motivate further research in the field of metabolomics to identify the metabolic pathways driving the enhancement of MDSCs in order to effectively target their ability to promote tumour development and progression.

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Section: Introductionmentioning

confidence: 99%

Energy metabolism manipulates the fate and function of tumour myeloid-derived suppressor cells

Pang

Lin

et al. 2019

Br J Cancer

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“…Immune cells undergo metabolic reprogramming in autoimmune and autoinflammatory diseases. This is also the case in SLE, where T cells are hyper-oxidative (52). T cells from SLE patients differ from activated T cells from healthy persons (53,54).…”

Section: Redox Metabolism In Sle T Cellsmentioning

confidence: 86%

Oxidative Stress in SLE T Cells, Is NRF2 Really the Target to Treat?

Ohl

Tenbrock

2021

Front. Immunol.

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Oxidative stress is a major component of cellular damage in T cells from patients with systemic lupus erythematosus (SLE) resulting amongst others in the generation of pathogenic Th17 cells. The NRF2/Keap1 pathway is the most important antioxidant system protecting cells from damage due to oxidative stress. Activation of NRF2 therefore seems to represent a putative therapeutic target in SLE, which is nevertheless challenged by several findings suggesting tissue and cell specific differences in the effect of NRF2 expression. This review focusses on the current understanding of oxidative stress in SLE T cells and its pathophysiologic and therapeutic implications.

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“…Area under the curve = 1.00, 95% confidence interval = 1.00-1.00, optimal cut-off 37.24 ng/ml. Vertical lines present the median and interquartile range pathways were recently proposed to play a crucial role in the activation of the immune system that drives autoimmune diseases including SLE [26,27]. A number of pathways found to be associated with autoimmunity and SLE have also been identified, including Fc gamma Rmediated phagocytosis and phagosome pathways [28,29].…”

Section: Discussionmentioning

confidence: 99%

Proteomic analysis in lupus mice identifies Coronin-1A as a potential biomarker for lupus nephritis

et al. 2020

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Background: Approximately 50% of systemic lupus erythematosus (SLE) patients develop nephritis, which is among the most severe and frequent complications of the disease and a leading cause of morbidity and mortality. Despite intensive research, there are still no reliable lupus nephritis (LN) markers in clinical use that can assess renal damage and activity with a high sensitivity and specificity. To this end, the aim of this study was to identify new clinically relevant tissue-specific protein biomarkers and possible underlying molecular mechanisms associated with renal involvement in SLE, using mass spectrometry (MS)-based proteomics. Methods: Kidneys were harvested from female triple congenic B6.NZMsle1/sle2/sle3 lupus mice model, and the respective sex-and age-matched C57BL/6 control mice at 12, 24 and 36 weeks of age, representing presymptomatic, established and end-stage LN, respectively. Proteins were extracted from kidneys, purified, reduced, alkylated and digested by trypsin. Purified peptides were separated by liquid chromatography and analysed by high-resolution MS. Data were processed by the Progenesis QIp software, and functional annotation analysis was performed using DAVID bioinformatics resources. Immunofluorescence and multiple reaction monitoring (MRM) MS methods were used to confirm prospective biomarkers in SLE mouse strains as well as human serum samples.

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Immune cell metabolism in autoimmunity

Cited by 27 publications

References 128 publications

Energy metabolism manipulates the fate and function of tumour myeloid-derived suppressor cells

Energy metabolism manipulates the fate and function of tumour myeloid-derived suppressor cells

Oxidative Stress in SLE T Cells, Is NRF2 Really the Target to Treat?

Proteomic analysis in lupus mice identifies Coronin-1A as a potential biomarker for lupus nephritis

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