title: Microbe- and danger-induced inflammation.
abstract: The ability of the immune system to give rise to an effective response against pathogens while maintaining tolerance towards self-tissues has always been an object of keen interest for immunologist. Over the years, different theories have been proposed to explain if and how the immune system is able to discriminate between self and non-self, including the Infectious Non-self theory from Charles Janeway and Polly Matzinger's Danger theory. Nowadays we know Janeway's theory is largely true, however the immune system does respond to injured, stressed and necrotic cells releasing danger signals (DAMPs) with a potent inflammatory response. To avoid unwanted prolonged autoimmune reactions, though, danger-induced inflammation should be tightly regulated. In the present review we discuss how prototypic DAMPs are able to induce inflammation and the peculiarity of danger-induced inflammation, as opposed to a complete immune response to fight pathogen invasions.
authors.affiliation: Department of Biotechnology and Biosciences, University of Milano-Bicocca, Piazza della Scienza 2, 20126 Milan, Italy.
authors.forename: Achille
authors.initials: A
authors.lastname: Broggi
authors.affiliation: Department of Biotechnology and Biosciences, University of Milano-Bicocca, Piazza della Scienza 2, 20126 Milan, Italy. Electronic address: francesca.granucci@unimib.it.
authors.forename: Francesca
authors.initials: F
authors.lastname: Granucci
mesh_terms: D000818:Animals; D001419:Bacteria / Q000276:immunology*; D024243:HMGB1 Protein / Q000378:metabolism; D006801:Humans; D058847:Inflammasomes / Q000378:metabolism; D007249:Inflammation / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D051192:Receptors, Pattern Recognition / Q000378:metabolism; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D024243:HMGB1 Protein; D058847:Inflammasomes; D051192:Receptors, Pattern Recognition; D051193:Toll-Like Receptors
keywords: Danger; HMGB1; Infections; Inflammasome; Inflammation; TLRs