Effects of altered glycolysis levels on CD8+ T cell activation and function

Cell Death and Disease, Год журнала: 2023, Номер 14(7)

Опубликована: Июль 8, 2023

CD8+ T cells are an important component of the body's adaptive immune response. During viral or intracellular bacterial infections, rapidly activated and differentiated to exert their function by producing cytokines. Alterations in glycolysis have effect on activation function, while is for cell functional failure recovery. This paper summarizes importance system. We discuss link between activation, differentiation, proliferation, altered function. In addition, potential molecular targets enhance restore affecting senescence summarized. review provides new insights into relationship proposes novel strategies immunotherapy targeting glycolysis.

Язык: Английский

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Ferroptosis of T cell in inflammation and tumour immunity

Clinical and Translational Medicine, Год журнала: 2025, Номер 15(3)

Опубликована: Март 1, 2025

Ferroptosis is an innovative concept defined as a distinct programmed cell death mode regulated by iron-dependent lipid peroxidation accumulation. This process governed numerous energy metabolites such fatty acids, amino acids and glucose, well iron homeostasis. In recent years, increasing studies have been devoted to the crucial effects of ferroptosis in immune cells during pathogenesis diseases infections, tumours autoimmune disorders. review summarises latest advancements T-cell ferroptosis, addresses key components mechanism T inflammatory conditions tumour progression, highlights potential target for treating related diseases. KEY POINTS: Ferroptosis-related mechanisms significantly affect biology CD4+ subsets are further involved Crosstalk between CD8+ induces microenvironment. Glutathione peroxidase 4 loss promotes regulatory enhance anti-tumour immunity.

Язык: Английский

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Spatiotemporal metabolomic approaches to the cancer-immunity panorama: a methodological perspective

Molecular Cancer, Год журнала: 2024, Номер 23(1)

Опубликована: Сен. 18, 2024

Язык: Английский

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COVID-19 and our understanding of vitamin D and immune function

The Journal of Steroid Biochemistry and Molecular Biology, Год журнала: 2025, Номер 249, С. 106710 - 106710

Опубликована: Фев. 20, 2025

The interaction between vitamin D and the immune system is perhaps most well recognised extraskeletal facet of D, encompassing early studies therapy for TB leprosy through to more recent links with autoimmune disease. However, spotlight on function has been particularly intense in last five years following COVID-19 pandemic. This was due, part, many association status infection disease prognosis, as smaller number clinical trials supplementation. a potential role also stemmed from basic biology that provides plausible mechanistic rationale beneficial effects improved health setting respiratory infection. aim this review summarise different strands evidence supporting effect COVID-19, how modified during pandemic itself, new aspects are likely arise near future. Key topics feature are: antibacterial versus antiviral innate responses 1,25-dihydroxyvitamin (1,25(OH)2D); 1α-hydroxylase (CYP27B1) activity metabolism 25-hydroxyvitamin (25(OH)D) beyond antigen-presenting cells; advances cell target gene (notably changes metabolic profile). Whilst much interest era focused public health, continued evolution our understanding interacts components continues support health.

Язык: Английский

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Immuno-cell metabolic changes in HIV-1 infection

Infectious Diseases & Immunity, Год журнала: 2025, Номер unknown

Опубликована: Март 12, 2025

Abstract Recent research has shown that metabolic processes within immune cells are essential for both human immunodeficiency virus 1 (HIV-1) infection and the response. Throughout HIV-1 infection—from acute stages to chronic viral latency—immune experience shifts in energy demands pathways, paralleling T-cell exhaustion. Dysregulated metabolism compromises cell function, leading dysfunction persistent inflammation. Therefore, alterations constitute a critical mechanism progression This review specifically explores profiles roles of T cells, monocytes-macrophages, dendritic natural killer B at different infection, emphasizing effects on pathways diverse types. These insights offer valuable therapeutic strategies aimed inhibiting replication, restoring controlling disease progression.

Язык: Английский

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Vitamin D Decreases Susceptibility of CD4+ T Cells to HIV Infection by Reducing AKT Phosphorylation and Glucose Uptake: A Bioinformatic and In Vitro Approach

Biomolecules, Год журнала: 2025, Номер 15(3), С. 432 - 432

Опубликована: Март 18, 2025

Activated immune cells are highly susceptible to human immunodeficiency virus (HIV) infection. Vitamin D (VitD) induces antimicrobial responses and reduces cellular activation. We investigated VitD effects on HIV-1 replication, glucose uptake, gene regulation using computational in vitro approaches. CD4+ T from healthy male donors were treated with infected HIV-1. After 72 h, p24 protein was measured assess viral replication. anti- pro-HIV genes analyzed by a Boolean network model based curated databases the literature. CCR5 CXCR4 coreceptor expression, AKT phosphorylation, uptake evaluated flow cytometry, expression of some model-identified quantified qPCR. reduced 53.2% (p = 0.0078). modeling predicted that upregulates antiviral, migration, cell-differentiation related genes, while downregulating activation, proliferation, metabolism, HIV notably AKT1, CCNT1, SLC2A1, HIF1A, PFKL. In vitro, phosphorylation 26.6% 0.0156), transcription CCNT1 22.7% 0.0391), 22.8% 0.0039) without affecting classic antiviral or expression. These findings suggest an anti-HIV effect VitD, mediated through metabolism downmodulation, both involved cell activation

Язык: Английский

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Computational modeling of metabolism in oncology

Elsevier eBooks, Год журнала: 2025, Номер unknown, С. 81 - 107

Опубликована: Янв. 1, 2025

Язык: Английский

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Andrographolide sulfonate alleviates rheumatoid arthritis by inhibiting glycolysis-mediated activation of PI3K/AKT to restrain Th17 cell differentiation

Chinese Journal of Natural Medicines, Год журнала: 2025, Номер 23(4), С. 480 - 491

Опубликована: Апрель 1, 2025

Язык: Английский

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Metabolic Reprogramming in HIV+ CD4+ T-Cells: Implications for Immune Dysfunction and Therapeutic Targets in M. tuberculosis Co-Infection

Metabolites, Год журнала: 2025, Номер 15(5), С. 285 - 285

Опубликована: Апрель 22, 2025

Background/Objectives: HIV and Mycobacterium tuberculosis (M.tb) co-infection presents a major global health burden. The immune response to M.tb is largely orchestrated by cluster of differentiation 4-positive (CD4+) T cells, with CD8+ cells playing an auxiliary role. This study aims investigate the immunometabolic CD4+ antigens, analysed using metabolomics, elucidate metabolic shifts that may influence function in HIV+ environment. Methods: Whole blood samples from newly diagnosed, treatment-naïve individuals were stimulated antigens early secreted antigenic target 6 (ESAT-6) culture filtrate protein 10 (CFP-10) QuantiFERON® (QFT) Gold Plus assay. Following incubation, plasma through untargeted nuclear magnetic resonance (1H-NMR) spectroscopy. Metabolomic data processed MetaboAnalyst, differential metabolites identified multivariate statistical analyses. Results: Metabolic profiling PBMCs revealed distinct differences between CD4+/CD8+ T-cell activation. exhibited enhanced glycolysis, elevated levels are linked Warburg effect. Additionally, vitamin D found correlate certain metabolites, suggesting role modulating responses. Conclusions: These findings suggest complex interplay cell metabolism activation individuals. demonstrates significantly influences broader profile peripheral mononuclear (PBMCs), highlighting altered pathways critical responses disease progression. contribute understanding immunometabolism emphasise need for further research into targeted interventions.

Язык: Английский

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Defective autophagy in CD4 T cells drives liver fibrosis via type 3 inflammation

Nature Communications, Год журнала: 2025, Номер 16(1)

Опубликована: Апрель 24, 2025

Conventional CD4 T cells represent a major source of inflammatory mediators that drive progression chronic liver disease to fibrosis and end-stage cirrhosis. Identification cell pathways limits the response could thus have therapeutic relevance. Here we show, using both human samples mouse models, autophagy is deficient in from patients with advanced fibrosis, loss following genomic deletion ATG5 associated emergence pathogenic IL-17A + IFN-γ Th17 mice. Mechanistically, lacking display glycolytic phenotype enhanced type 3 cytokine (i.e., GM-CSF) release, shifting hepatic myofibroblasts, hepatocytes macrophages toward proinflammatory phenotype. We also show can be rescued extensive leading decreased frequency reduced GM-CSF levels; addition, limited observed mice which Rubicon, negative regulator autophagy, deleted specifically their cells. Our findings implicate as key target control inflammation-driven during injury.

Язык: Английский

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