Immune system articles from across Nature Portfolio

Carbon-containing particulates accumulate with age in a subset of macrophages in human lung-associated lymph nodes, decrease macrophage phagocytic capacity and turnover and disrupt lymphoid tissue structure, potentially compromising adaptive immune responses.

Asplenia and hyposplenism can have multiple and complex causes and lead to morbidity and mortality, especially owing to overwhelming post-splenectomy infections. In this Primer, Lenti and colleagues review epidemiology, pathophysiology, diagnosis and management of these conditions, and discuss patient quality of life and future strategies.

Accumulating evidence supports the critical role of T cells as drivers and modifiers of atherosclerosis. In this Review, Ley and colleagues describe the latest advances in our understanding of the role of T cell subsets in atherosclerosis, discuss the process of T cell homing to atherosclerotic plaques and highlight potential T cell-related therapies for atherosclerosis.

Naturally occurring cationic host defence peptides, also known as antimicrobial peptides, can control infections by their direct microbicidal properties and by modulating the host’s immune responses. In addition, certain cationic host defence peptides can resolve harmful inflammation. Here, Mookherjee et al. assess the emerging potential to therapeutically harness these peptides to treat infectious diseases, chronic inflammatory disorders and wound healing, highlighting current preclinical studies and clinical trials.

Results of a new study indicate that eosinophils have a role in maintaining bone homeostasis through their inhibitory effects on bone-resorbing osteoclasts.

An approach that increases the expression of the chemokine receptor CXCR4 in vascular cells by targeting a microRNA-based repressive pathway attenuates atherosclerosis in mice and promotes atheroprotective functions in human and mouse vascular cells in vitro.

A new study reveals that the disrupted sleep patterns that are frequently observed in patients with cardiac disease are driven by immune-mediated sympathetic denervation and dysfunction of the pineal gland, which leads to a decrease in the circulating levels of melatonin and subsequent sleep disruption.