The sterile inflammatory response

By K. Rock, E. Latz, Fernando Ontiveros, H. Kono. Annual Review of Immunology, 2010

884 citations recorded by the source corpus.

The acute inflammatory response is a double-edged sword. On the one hand it plays a key role in initial host defense particularly against many infections. On the other hand its aim is imprecise and as a consequence, when it is drawn into battle, it can cause collateral damage in tissues. In situations where the inciting stimulus is sterile, the cost-benefit ratio may be high; because of this, sterile inflammation underlies the pathogenesis of a number of diseases. While there have been major advances in our understanding of how microbes trigger inflammation, much less has been learned about this process in sterile situations. 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. Although this subset of stimuli is structurally very diverse and might appear to be unrelated, there is accumulating evidence that the innate immune system may recognize them in similar ways and stimulate the sterile inflammatory response via common pathways. Here we review established and emerging data about these responses.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4239bf095ca8a64bcd270d4b13efcaf1a1fbd277

How researchers see this paper

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In Immunology

1. P. Kubes
2. M. Pinzani
3. M. Phillipson
4. J. Ting

In Molecular Biology

1. B. Davis
2. Haitao Wen
3. P. Kubes
4. M. Phillipson
5. J. Ting

Citations in the corpus

• The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases (2011, background): “Self NLRP3 activators include ATP, monosodium urate (MSU), calcium pyrophosphate dihydrate (CPPD), cholesterol crystals, amyloid β, hyaluron, and possibly glucose (26).”
• The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “[64] Rock KL, Latz E, Ontiveros F, et al.”
• The adapter MAVS promotes NLRP3 mitochondrial localization and inflammasome activation (2013, neutral): “In addition, the NLRP3 inflammasome has been implicated in the inflammatory response to dying cells in the absence of infection (Rock et al., 2010).”
• The neutrophil in vascular inflammation (2011, background): “DAMPs and pathogen-associated molecular patterns function similarly, both stimulating pattern recognition receptors such as TLRs or NOD-like receptors (NLRs) [62] [63] [64] .”