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Diverse components of the tumor microenvironment affect T cell metabolism in ways that are crucial to improving immunotherapy.

Macrophage Bmal1 controls the timing of the glycolytic to oxidative metabolism transition that dictates the extent of Hif-1a activation and the associated inflammatory response.

Ketogenic diet protects against coronavirus-infected aged mice, which, like humans, are significantly more susceptible to infections, by deactivating NLRP3 inflammasome, reducing pathogenic monotypes, and expanding γδ T cells in the lung.

SIRT1 and SIRT3-mediated immunometabolic shift governs intracellular Salmonella proliferation both in vitro and in vivo and dissemination in mice, thereby influencing the infection outcomes.

In-depth proteomic analyses of intestinal tissue-resident intraepithelial T lymphocytes reveals how these cells are adapted to the intestinal environment through increased cholesterol and lipid metabolism, tailored metabolic profiles, receptors for interacting with epithelial cells, and tightly regulated signalling pathways.

Diet-induced obesity in mice led to a duration of diet-dependent bone marrow adipocyte whitening, which drove monocyte expansion and skewing towards a tissue-invasive phenotype, likely contributing to ensuing tissue infiltration that accompanies obesity and diabetes.

Type 2 cytokines induce macrophage innate training, where enhanced pro-inflammatory responses are fuelled by oxidative phosphorylation rather than aerobic glycolysis.

Complex I of the mitochondrial respiratory chain is necessary for interferon gamma-mediated responses in antigen-presenting cells and is required for CD4+ T cell activation.