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Innate immune cells are white blood cells that mediate innate immunity and include basophils, dendritic cells, eosinophils, Langerhans cells, mast cells, monocytes and macrophages, neutrophils and NK cells.
Atrial fibrillation is linked to fibrosis and inflammatory macrophage recruitment in atria, with osteopontin (encoded by Spp1) increasing susceptibility by promoting atrial fibrosis and uneven conduction. Research shows that antibody-based silencing of Spp1 in some TREM2+ macrophages reduces fibrotic remodeling and atrial fibrillation risk.
Group 3 innate lymphoid cells (ILC3s) are key regulator of intestinal immunity. However, whether these cells drive necrotizing enterocolitis (NEC) and through which mechanism remains unexplored. Here, the authors employ a mouse model of neonatal NEC and implicate NKp46⁻CCR6⁻ double negative ILC3 autophagy in pathogenic ILC3 expansion and activation during NEC via HIF1a-modulation of glycolipid metabolism.
Maternal obesity is a risk factor for developing chronic kidney disease in the offspring later in life. Here the authors study male offspring in a mouse model of maternal obesity and identify dysregulated metabolism due to disrupted crosstalk between proximal tubules and macrophages as an important mechanism.
Immunosuppressive tumor-associated macrophages (TAM) contribute to resistance to immune checkpoint blockade. Here, the authors propose BCAT1 to inhibit crotonate-mediated epigenetic reprogramming of tumor-associated macrophages, with BCAT1 loss promoting immune escape in hepatocellular carcinoma mouse models.
Innate lymphoid cells (ILCs) influence rheumatoid arthritis by amplifying inflammatory circuits through ILC3 activity and promoting immune regulation via ILC2 responses. These context-dependent functions position ILC subsets as emerging biomarkers and targets for innovative therapies.
Macrophages continuously ‘nibble’ healthy neighbouring cells, capturing minute amounts of cytosolic material that are preserved in specialized vesicles and preferentially routed for cross-presentation to CD8+ T cells.
Atrial fibrillation is linked to fibrosis and inflammatory macrophage recruitment in atria, with osteopontin (encoded by Spp1) increasing susceptibility by promoting atrial fibrosis and uneven conduction. Research shows that antibody-based silencing of Spp1 in some TREM2+ macrophages reduces fibrotic remodeling and atrial fibrillation risk.
Engineered immunosuppressive and fibrosis-targeted dendritic cells protect against pathological cardiac remodelling in animal models of ischaemic and pressure-overload-induced heart failure, including a non-human primate model of myocardial infarction.
In this issue of Nature Metabolism, Diotallevi et al. propose a novel non-canonical function of inducible nitric oxide synthase (iNOS) as a regulator of immune-responsive gene 1 (IRG1, also known as ACOD1) enzymatic activity and the IRG1 protein interactome.
