The Danger Model: A Renewed Sense of Self

By P. Matzinger. Science, 2002

4,431 citations recorded by the source corpus.

Subfields: Biomedical Engineering, Immunology, Infectious Diseases

View Paper: https://www.semanticscholar.org/paper/181c3b5ccbbe9f02d666fd9796988fd5df221fb8

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biomedical Engineering

In Immunology

In Infectious Diseases

Citations in the corpus

Inflammatory signals in dendritic cell activation and the induction of adaptive immunity (2009, background): “According to the danger model, APCs are activated to prime adaptive immune responses by danger signals derived from stressed or injured cells (19, 73).”
HMGB1: Endogenous Danger Signaling (2008, background): “In this model, initiation of the inflammatory response occurs in response to molecular patterns that are associated with both pathogens and some normal cellular components that are released by damaged cells during both infectious and sterile processes (4).”
Variation in immune defence as a question of evolutionary ecology (2003, background): “For this, presumably, appropriate cofactors are required (Matzinger 2002).”
IMMUNE TOLERANCE INDUCTION BY APOPTOTIC CELLS REQUIRES CASPASE-DEPENDENT OXIDATION OF HMGB1 (2008, background): “Should cell death due to damage or infection occur, antigen stimulation would be limited only to neoantigens present at the site because tolerance induced by ongoing apoptosis would eliminate responses to self-antigens (Matzinger, 2002) (Ferguson et al.”
Pyroptosis: host cell death and inflammation (2009, background): “TLRs and NLRs The host can use a range of mechanisms to sense intracellular and extracellular 'danger' signals generated by invading pathogenic microorganisms or by the host in response to tissue injur”
Adoptive-cell-transfer therapy for the treatment of patients with cancer (2003, background): “The tumour environment could lack a 'danger signal' or other innate immune stimulation, preventing a general inflammatory reaction from evolvin”
NLRP3 inflammasome: From a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases (2015, neutral): “This is an open access article u adipose tissue macrophages; ATP, domain; CARD, caspase recruitmen drome; CPPD, calcium pyrophosph nflammatory syndrome; FCU, fami eptide; IL-1β, Interleukin-1β; IL-1 R ceptor; MDP, muramyl dipeptide; main; NLRP3, nucleotide-binding atal-onset multisystem inflammato c”