The Danger Model Approach to the Pathogenesis of the Rheumatic Diseases
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 traditio...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2015/506089 |
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| _version_ | 1832552916881244160 |
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| author | César Pacheco-Tena Susana Aideé González-Chávez |
| author_facet | César Pacheco-Tena Susana Aideé González-Chávez |
| author_sort | César Pacheco-Tena |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-60a6e7fb02d640cda6a72471c957d8d3 |
| institution | Kabale University |
| issn | 2314-8861 2314-7156 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Immunology Research |
| spelling | doaj-art-60a6e7fb02d640cda6a72471c957d8d32025-02-03T05:57:27ZengWileyJournal of Immunology Research2314-88612314-71562015-01-01201510.1155/2015/506089506089The Danger Model Approach to the Pathogenesis of the Rheumatic DiseasesCésar Pacheco-Tena0Susana Aideé González-Chávez1Facultad de Medicina, Universidad Autónoma de Chihuahua, Circuito No. 1, Nuevo Campus Universitario, 31240 Chihuahua, CHIH, MexicoFacultad de Medicina, Universidad Autónoma de Chihuahua, Circuito No. 1, Nuevo Campus Universitario, 31240 Chihuahua, CHIH, MexicoThe 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.http://dx.doi.org/10.1155/2015/506089 |
| spellingShingle | César Pacheco-Tena Susana Aideé González-Chávez The Danger Model Approach to the Pathogenesis of the Rheumatic Diseases Journal of Immunology Research |
| title | The Danger Model Approach to the Pathogenesis of the Rheumatic Diseases |
| title_full | The Danger Model Approach to the Pathogenesis of the Rheumatic Diseases |
| title_fullStr | The Danger Model Approach to the Pathogenesis of the Rheumatic Diseases |
| title_full_unstemmed | The Danger Model Approach to the Pathogenesis of the Rheumatic Diseases |
| title_short | The Danger Model Approach to the Pathogenesis of the Rheumatic Diseases |
| title_sort | danger model approach to the pathogenesis of the rheumatic diseases |
| url | http://dx.doi.org/10.1155/2015/506089 |
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