A new study shows that inflammation spreads from psoriatic skin to joint disease through the migration of skin myeloid precursors to the joints, where they can become inflammatory macrophages unless they are kept in check by resident regulatory fibroblasts.
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.
Early life exposure to allergens triggers a unique mode of dendritic cell activation in the skin, inducing local inflammation and priming systemic allergic responses to subsequent exposures in later life.
A previously unappreciated sympathetic–immune axis links psychological stress to eosinophil recruitment and consequent worsening of atopic dermatitis.
Functional profiling of autoantibodies from individuals with long COVID demonstrates a casual link with neurological symptoms, reframing long COVID as, at least in part, an antibody-mediated disease.
A study shows that transient blockade of type I interferon signalling during T cell priming enhances the generation of stem cell-like memory CD8+ T cells after viral infection and mRNA vaccination.
B cells that expand following infection with EBV can colonize the brain, where they recruit activated T cells that have potential to cause neuronal damage, thereby providing a mechanism to explain the link between EBV and increased MS risk.
Microglia are not confined to the central nervous system but are also present in the periphery, wrapped around large neuronal somas of humans and larger animals but not small animals like mice.
A study describes how maternal immune activation can lead to neurodevelopmental deficits in offspring, through a mechanism involving granzyme B release by decidual natural killer cells.
Besides killing infected or transformed cells, interferon-activated natural killer cells can kill T follicular helper cells and may contribute to poor antibody responses in some individuals infected with SARS-CoV-2.
The antitumoural effects of BCG can be vastly improved by combining it with β-glucan. The combination therapy enhances granulopoiesis and trains neutrophils to resist conversion into a protumoural phenotype in a mouse model of bladder cancer.
Lipid transport regulates activation of intestinal T helper 17 cells and thereby limits dietary fat absorption and diet-induced weight gain.
To evade elimination by T cells, tumour cells transfer mutant mitochondria to T cells, which reprogrammes their metabolism and compromises their antitumour activity.
Sex hormones in male mice negatively regulate type 2 innate lymphoid cells in the skin, impairing the induction and activation of dendritic cells and thereby contributing to differences in immunity in males and females.
Investigation of neutrophil heterogeneity in tumours reveals the irreversible programming of long-lived, pro-angiogenic neutrophils that drive tumour progression.
Transient depletion of the gut microbiome by antibiotics in early life reduces systemic levels of the metabolite indole-3-propionic acid, which causes long-lasting mitochondrial damage to lung epithelial cells and increases susceptibility to airway inflammation in adult mice.
Sialylated IgG protects against severe influenza by inducing the transcriptional repressor REST, which dampens the inflammatory response and preserves lung tissue function.
CD8+ T cells become exhausted when exposed to the mechanical forces of stiff solid tumours, owing to signalling through the transcription factor OSR2.
Age-associated defects in dendritic cells can be corrected by hyperactivating adjuvants containing an oxidized phospholipid to induce effective antitumour responses in mice.
Febrile temperatures disrupt metabolism and induce DNA damage disproportionately in T helper 1 cell subsets. Cells that survive apoptosis and adapt by increasing their mitochondrial mass and DNA damage responses gain enhanced effector functions.
