ReviewJournal of immunology research2015
The danger model approach to the pathogenesis of the rheumatic diseases.
Review in Journal of immunology research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Oxidative Stress Relevance in the Pathogenesis of the Rheumatoid Arthritis: A Systematic Review.BioMed research international · 2016Pooled it
- Inflammatory Arthritis and the Environment: Causes and Consequences of Spondyloarthritis.Journal of personalized medicine · 2025Review
- Fostering tissue engineering and regenerative medicine to treat musculoskeletal disorders in bone and muscle.Bioactive materials · 2024Review
- Article
- Article
- Polyphenols Targeting MAPK Mediated Oxidative Stress and Inflammation in Rheumatoid Arthritis.Molecules (Basel, Switzerland) · 2021Review
- Neuroinflammation: An Integrating Overview of Reactive-Neuroimmune Cell Interactions in Health and Disease.Mediators of inflammation · 2021Review
- Living in a Hostile World: Inflammation, New Drug Development, and Coronavirus.Frontiers in immunology · 2020Review
- DNA Damage and Deficiencies in the Mechanisms of Its Repair: Implications in the Pathogenesis of Systemic Lupus Erythematosus.Journal of immunology research · 2018Review
- High prevalence of autoimmune disease in the rare inflammatory bone disorder sternocostoclavicular hyperostosis: survey of a Dutch cohort.Orphanet journal of rare diseases · 2017Article
- Hypoxia and its implications in rheumatoid arthritis.Journal of biomedical science · 2016Review
- Serum levels of HSP70 and other DAMP proteins can aid in patient diagnosis after traumatic injury.Cell stress & chaperones · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The danger model was proposed by Polly Matzinger as complement to the traditional self-non-self- (SNS-) model to explain the immunoreactivity. The danger model proposes a central role of the tissular cells' discomfort as an element to prime the immune response processes in opposition to the traditional SNS-model where foreignness is a prerequisite. However recent insights in the proteomics of diverse tissular cells have revealed that under stressful conditions they have a significant potential to initiate, coordinate, and perpetuate autoimmune processes, in many cases, ruling over the adaptive immune response cells; this ruling potential can also be confirmed by observations in several genetically manipulated animal models. Here, we review the pathogenesis of rheumatic diseases such as systemic lupus erythematous, rheumatoid arthritis, spondyloarthritis including ankylosing spondylitis, psoriasis, and Crohn's disease and provide realistic approaches based on the logic of the danger model. We assume that tissular dysfunction is a prerequisite for chronic autoimmunity and propose two genetically conferred hypothetical roles for the tissular cells causing the disease: (A) the Impaired cell and (B) the paranoid cell. Both roles are not mutually exclusive. Some examples in human disease and in animal models are provided based on current evidence.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.