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Monocytes and macrophages are myeloid cells that have important innate immune functions. Macrophages reside in tissues and respond to infection by producing inflammatory mediators and engulfing bacteria. Monocytes are recruited to inflamed tissues and can produce inflammatory mediators or differentiate into macrophages. Both cells types can also promote tissue repair.
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.
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.
Here the researchers report that 5’tRFGlu(CTC), a tRNA-derived fragment, is associated with diabetes and mediates pancreatic beta cell and macrophage responses to nutritional stress. targeted inhibition of 5’tRFGlu(CTC) preserves beta cell viability and function under lipotoxic exposure.
Tick saliva reprograms macrophages into immunosuppressive hubs that suppress T cell responses and promote IL-10–producing CD4⁺ T cells, revealing a macrophage-dependent mechanism of tick-induced immune modulation in the skin.
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.
Fibroblasts and macrophages have classically been viewed as engaging in a one-way supportive relationship in which fibroblasts sustain macrophage survival. Emerging evidence now challenges this paradigm by demonstrating a bidirectional regulatory circuit in which macrophages actively restrain fibroblast activation to preserve tissue integrity.
