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Comparative lipidomic and transcriptomic profiling reveals distinct fatty acid utilization in T and B cells across mouse and human

ABSTRACT: Lipid metabolism is increasingly recognized as a critical determinant of immune cell differentiation and function, yet the metabolic programs that distinguish closely related adaptive immune cell subsets remain incompletely defined. Here we demonstrate that T and B cells employ distinct fatty acid utilization strategies across species. Integrated lipidomic and transcriptomic analyses of mouse and human lymphocytes revealed enrichment of long-chain phospholipid species in T cells, including prominent increases in arachidonic acid–containing lipids, accompanied by elevated expression of fatty acid elongation–associated genes including Elovl5. In contrast, B cells preferentially accumulated phospholipids with shorter and/or more unsaturated acyl chains, notably with consistent enrichment of eicosapentaenoic acid–containing lipids, together with increased expression of genes involved in fatty acid uptake, desaturation, and phospholipid remodeling, including Cd36, Scd1, and Lpgat1. Acyl-chain pairing analyses further uncovered distinct organizational patterns in lipid assembly, and cross-species comparisons revealed both conserved features and marked species-specific divergence, highlighting shared metabolic principles in mouse and human lymphocytes. Our data indicate that differential fatty acid elongation, uptake, and remodeling programs shape lineage-specific lipid architectures and contribute to metabolic specialization in adaptive immune cells.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE326689 | GEO | 2026/06/30

REPOSITORIES: GEO

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Project description:vanEunen2013 - Network dynamics of fatty acid β-oxidation (time-course model) Lipid metabolism plays an important role in the development of metabolic syndrome, a major risk factor for cardiovascular disease and diabetes. This model gives insights into the response of lipid oxidation to dietart and medical interventions. The model predicts the rate of lipid oxidation and the time course of most acyl carnitines. There are two models described in the paper, (i) steady-state model [ BIOMD0000000505 ], (ii) time-course model [ BIOMD0000000506 ]. This model corresponds to the time-course model. This model is described in the article: Biochemical competition makes fatty-acid β-oxidation vulnerable to substrate overload. van Eunen K, Simons SM, Gerding A, Bleeker A, den Besten G, Touw CM, Houten SM, Groen BK, Krab K, Reijngoud DJ, Bakker BM. PLoS Comput Biol. 2013;9(8):e1003186. Abstract: Fatty-acid metabolism plays a key role in acquired and inborn metabolic diseases. To obtain insight into the network dynamics of fatty-acid β-oxidation, we constructed a detailed computational model of the pathway and subjected it to a fat overload condition. The model contains reversible and saturable enzyme-kinetic equations and experimentally determined parameters for rat-liver enzymes. It was validated by adding palmitoyl CoA or palmitoyl carnitine to isolated rat-liver mitochondria: without refitting of measured parameters, the model correctly predicted the β-oxidation flux as well as the time profiles of most acyl-carnitine concentrations. Subsequently, we simulated the condition of obesity by increasing the palmitoyl-CoA concentration. At a high concentration of palmitoyl CoA the β-oxidation became overloaded: the flux dropped and metabolites accumulated. This behavior originated from the competition between acyl CoAs of different chain lengths for a set of acyl-CoA dehydrogenases with overlapping substrate specificity. This effectively induced competitive feedforward inhibition and thereby led to accumulation of CoA-ester intermediates and depletion of free CoA (CoASH). The mitochondrial [NAD⁺]/[NADH] ratio modulated the sensitivity to substrate overload, revealing a tight interplay between regulation of β-oxidation and mitochondrial respiration. This model is hosted on BioModels Database and identified by: BIOMD0000000506 . To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Comparative lipidomic and transcriptomic profiling reveals distinct fatty acid utilization in T and B cells across mouse and human

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