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Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization
TLDR
It is demonstrated that silica and aluminum salt crystals activated inflammasomes formed by the cytoplasmic receptor NALP3, which senses lysosomal damage as an endogenous 'danger' signal.
NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
TLDR
This corrects the article to show that the method used to derive the H2O2 “spatially aggregating force” is a two-step process, not a single step, like in the previous version of this paper.
How dying cells alert the immune system to danger
TLDR
Current knowledge of cell death and repair processes in the host and their importance to host defence and disease pathogenesis has only been appreciated relatively recently is reviewed.
Molecular identification of a danger signal that alerts the immune system to dying cells
TLDR
Uric acid stimulates dendritic cell maturation and, when co-injected with antigen in vivo, significantly enhances the generation of responses from CD8+ T cells, and have important implications for vaccines, autoimmunity and inflammation.
The sterile inflammatory response.
TLDR
This review focuses on a subset of the many sterile stimuli that can induce inflammation-specifically dead cells and a variety of irritant particles, including crystals, minerals, and protein aggregates.
Cloned dendritic cells can present exogenous antigens on both MHC class I and class II molecules.
TLDR
It is established that dendritic cells can present exogenous Ags on MHC class I molecules and appear to use a similar phagosome to cytosol pathway as macrophages, which is likely to play an important role in generating immune responses to tissue transplants and tumors in vivo.
Identification of a key pathway required for the sterile inflammatory response triggered by dying cells
TLDR
It is suggested that inhibiting the IL-1R–Myd88 pathway in vivo could block the damage from acute inflammation that occurs in response to sterile cell death, and do so in a way that might not compromise tissue repair or host defense against pathogens.
NLRP3 inflamasomes are required for atherogenesis and activated by cholesterol crystals that form early in disease
TLDR
It is shown that cholesterol crystals activate the NLRP3 inflammasome in phagocytes in vitro in a process that involves phagolysosomal damage and that crystalline cholesterol acts as an endogenous danger signal and its deposition in arteries or elsewhere is an early cause rather than a late consequence of inflammation.
Degradation of cell proteins and the generation of MHC class I-presented peptides.
TLDR
Recent discoveries about the proteolytic systems that degrade cell proteins are reviewed, how the ubiquitin-proteasome pathway generates the peptides presented on MHC-class I molecules, and how this process is stimulated by immune modifiers to enhance antigen presentation are reviewed.
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