News & Comment

Christoph Hess describes a 1984 paper by Barry Marshall and Robin Warren that proposed that bacteria might be a key factor in chronic gastritis.

Trifunctional antibodies, binding to the natural killer cell receptors NKp46 and CD16, as well as a tumour antigen, show promising activity in preclinical experiments.

Antibodies that dissolve Charcot–Leyden crystals may have therapeutic potential in asthma and other eosinophil-associated inflammatory diseases.

A new study identifies an unexpected role for type I interferon-responsive CD8⁺ T cells in cachexia associated with viral infection.

The response to anti-PD1 therapy depends on the expression of CXCR3 ligands by dendritic cells in the tumour, which promote the proliferation and activation of intratumoural CD8⁺ T cells.

Expression of VCAM1 on brain endothelium increases with age and targeting VCAM1 reverses microglial cell activation and cognitive deficits in older mice.

Betty Wu-Hsieh describes a 2013 paper by Gordon Brown and colleagues that showed fungal strain-specific interactions with the innate immune system.

Two new studies identify the discrete stromal cell subtypes that produce IL-33 in adipose tissue to support the immune cells that maintain adipose tissue homeostasis.

An intestinal mucus-dwelling bacterial species can trigger spontaneous colitis in mice lacking genes associated with Crohn’s disease.

This study shows that circular RNAs that contain double-stranded regions can modulate innate immunity by inhibiting the pattern recognition receptor protein kinase R (PKR).

A new study describes how mechanical skin injury caused by scratching can promote food anaphylaxis by increasing the number of mast cells in the gut through a keratinocyte–ILC2–tuft cell pathway.

Computational modelling predicts a co-stimulatory role for Toll-like receptor 5 (TLR5) in naive CD4⁺ T cell activation.

To maintain homeostasis and minimize unnecessary, potentially damaging inflammatory responses, tissue-resident macrophages cloak small tissue lesions to prevent neutrophil activation.

Two new studies show that the inflammasome protein NLRP1B becomes activated in response to pathogen-induced proteasomal degradation of its N-terminal fragment, thereby acting as a sensor of its own stability.

This study identifies a role for group 3 innate lymphoid cells in IL-2 production in the small intestine to maintain intestinal homeostasis through effects on regulatory T cells.

During inflammation, IL-17 rewires metabolic processes in lymph node fibroblastic reticular cells, thereby supporting their survival and population expansion.

Liver macrophages produce the non-inflammatory factor IGFBP7, which has direct effects on liver metabolism in metabolic disease without requiring a switch to a pro-inflammatory phenotype.

Tumour cells induce membrane cholesterol efflux from macrophages, leading to macrophage acquisition of a pro-tumour phenotype.

A new study shows that immune activation after infection involves competition for energy with physiological programmes such as maintaining a normal body temperature. This trade-off favours immune tolerance as a strategy for host defence.

Doreen Cantrell describes a 2005 paper by Graham Hardie and colleagues showing that Ca²⁺–calmodulin-dependent protein kinase kinases could phosphorylate and activate AMPK, which suggested a biochemical link between T cell receptor signalling and ATP production.