David Brough

This study uses reporter mice to visualise NLRP3 inflammasomes in vivo, revealing their localisation, organisation, and cellular sources.

This study shows that deleting microglial IL-1β improves acute stroke outcomes and modulates neurogenesis, with effects more pronounced in females.

This study shows that cell volume changes in macrophages enhance type I interferon signaling and inflammation through a DNA- and STING-dependent mechanism.

This study disrupts the nuclear localisation sequence of endogenous IL-1α in mice and examines its effects on inflammatory responses, finding no significant changes in LPS-induced transcriptional signatures or IL-1 release.

This study shows that cerebral ischaemic stroke alters mucosal IgA responses and host-commensal microbiota interactions, leading to changes in intestinal microbiota composition.

This study investigates how lysosome positioning affects NLRP3 inflammasome activation in HeLa and macrophage cells, finding that peripheral lysosome positioning enhances inflammasome activation.

This study shows the NLRP3 inflammasome is crucial for IL-18 production in a murine model of MAS but not for other disease features.

This study uses imaging mass cytometry to analyze spatial immunological differences in vestibular schwannomas from NF2 SWN patients, revealing niche-dependent T-cell regulation.

This study investigates the role of microglial-derived IL-1 in experimental ischemic stroke, finding it does not affect acute damage but influences neurorepair and functional recovery.

This study identifies brazilin as a natural product inhibitor of the NLRP3 inflammasome, effective in multiple models and suggesting its potential as a therapeutic scaffold.

The paper re-evaluates the efficiency of a CRISPR-Cas9 method for generating conditional knockout alleles in mice, finding very low success rates and high rates of undesired alleles.