Phagocytes articles from across Nature Portfolio

Cancer cells evade the immune system by disrupting phagocytic clearance. Here, the authors identify CD37 as a potential checkpoint molecule expressed on non-phagocytes and propose that binding to tumor-derived MIF reduces the phagocytic ability via inhibiting the AKT pathway. In preclinical mouse models, anti-CD37-based therapy enhances phagocytosis by macrophages, facilitating tumor clearance.

Phytic acid suppresses macrophage inflammation during Echinococcus multilocularis infection by chelating calcium, revealing a protein-independent immune evasion strategy that facilitates parasite survival.

Macrophages are crucial regulators of fibrosis. Here the authors describe how distinct subsets of monocytes and macrophages cooperate with fibroblasts across tissues to control progression from inflammation to fibrosis.

During tissue injury blood cells in the microvasculature and tissue resident cells have differing phenotypes. Here the authors use single cell transcriptomics in mice models to assess the differences in phenotype of immune cells in multiple organs and the tissue resident cells before, after and during acute kidney infection.

Phagocytosed bacteria can serve as an alternative nutrient source for macrophages, influencing their metabolic and immune responses through the recycling of microbial components, with the process regulated by nutrient-sensing mechanisms and bacterial viability.

Accumulation of inhaled carbon particulates in lung-draining lymph nodes with age impairs respiratory immunity.

Immune cells can promote the thermogenic phenotype of white adipocytes during cold exposure, in a process known as ‘browning’ or ‘beiging’. Wang et al. now reveal a potential mechanism whereby alternatively activated macrophages prompt adipose sympathetic nerve fibres to release norepinephrine and promote adipocyte beiging.

The retention of erythroid mitochondria, a feature associated with impairments in the ubiquitin–proteasome system, is detected in a subset of pediatric patients with lupus and is associated with the type I interferon pathway.