ASC and NLRP3 impair host defense during lethal pneumonia caused by serotype 3 Streptococcus pneumoniae in mice.
van Lieshout, Miriam H P; de Vos, Alex F; Dessing, Mark C; de Porto, Alexander P N A; de Boer, Onno J; de Beer, Regina; Terpstra, Sanne; Florquin, Sandrine; Van't Veer, Cornelis; van der Poll, Tom.
Eur J Immunol
; 48(1): 66-79, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-28971472
The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response.
The adaptor ASC has extracellular and 'prionoid' activities that propagate inflammation.
NLRP3 and ASC differentially affect the lung transcriptome during pneumococcal pneumonia.
Inflammasome-dependent Mechanisms Involved in Sensing and Restriction of Bacterial Replication.
NLRP3 activation and mitosis are mutually exclusive events coordinated by NEK7, a new inflammasome component.
The NLRP3 inflammasome is active but not essential in endotoxin-induced uveitis.
An additional piece in the puzzle of neutrophil-derived IL-1ß: the NLRP3 inflammasome.
The PYHIN Protein p205 Regulates the Inflammasome by Controlling Asc Expression.
Phosphorylation of the adaptor ASC acts as a molecular switch that controls the formation of speck-like aggregates and inflammasome activity.