Nature's choice of genes controlling chronic inflammation.
(2007) Symposium on Immunotherapy 2020 - Visions and Trends for Targeting Inflammatory Disease 4. p.1-15- Abstract
- Inflammation is a physiological response that may go uncontrolled and thereby develop in a chronic way. This seems to happen in many common diseases of autoimmune, degenerative, or allergic character. Rheumatoid arthritis (RA) is by definition a chronic disease with an autoimmune inflammatory attack on diarthrodial cartilaginous joints. The development of new treatment neutralizing cytokines involved in the inflammatory attack has given relief and gives the promise of more effective treatment of already established disease. It is now time to set our eyes on a new vision to develop preventive and curative treatment based on knowledge of the unique and causative pathogenic mechanisms. To do this we believe it is important to identify the... (More)
- Inflammation is a physiological response that may go uncontrolled and thereby develop in a chronic way. This seems to happen in many common diseases of autoimmune, degenerative, or allergic character. Rheumatoid arthritis (RA) is by definition a chronic disease with an autoimmune inflammatory attack on diarthrodial cartilaginous joints. The development of new treatment neutralizing cytokines involved in the inflammatory attack has given relief and gives the promise of more effective treatment of already established disease. It is now time to set our eyes on a new vision to develop preventive and curative treatment based on knowledge of the unique and causative pathogenic mechanisms. To do this we believe it is important to identify the natural-selected polymorphisms that are associated with disease. These have proven to be extremely difficult to identify in complex diseases such as RA, but using animal models, this work is closer to reality. Animal models have recently been developed mimicking various aspects of the human disease. We will present an example in which a genetic polymorphism associated with the development of arthritis has been identified. On the basis of this finding, a new pathway involving control of immune tolerance by reactive oxidative species has been identified and a new class of anti inflammatory agents activating the induced oxidative burst protein complex is suggested. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/607926
- author
- Holmdahl, Rikard LU
- organization
- publishing date
- 2007
- type
- Chapter in Book/Report/Conference proceeding
- publication status
- published
- subject
- keywords
- NADPH Oxidase: physiology, Reactive Oxygen Species, Chronic Disease, Rheumatoid: genetics, Arthritis, Animals, Rheumatoid: drug therapy, Animal, Disease Models, Genetic Predisposition to Disease, NADPH Oxidase: genetics, Humans, Major Histocompatibility Complex
- host publication
- Immunotherapy in 2020 - Visions and Trends for Targeting Inflammatory Disease (Ernst Schering Foundation Symposium)
- volume
- 4
- pages
- 1 - 15
- publisher
- Springer
- conference name
- Symposium on Immunotherapy 2020 - Visions and Trends for Targeting Inflammatory Disease
- conference location
- Potsdam, Germany
- conference dates
- 2006-10-22 - 2006-10-24
- external identifiers
-
- wos:000249018200001
- ISSN
- 0947-6075
- ISBN
- 978-3-540-70850-6
- DOI
- 10.1007/2789_2007_036
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medical Inflammation Research (013212019)
- id
- a0404f69-cb23-4e7b-ba03-40f893ef3c20 (old id 607926)
- alternative location
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17824178&dopt=Abstract
- date added to LUP
- 2016-04-01 15:32:34
- date last changed
- 2018-11-21 20:35:00
@inproceedings{a0404f69-cb23-4e7b-ba03-40f893ef3c20,
abstract = {{Inflammation is a physiological response that may go uncontrolled and thereby develop in a chronic way. This seems to happen in many common diseases of autoimmune, degenerative, or allergic character. Rheumatoid arthritis (RA) is by definition a chronic disease with an autoimmune inflammatory attack on diarthrodial cartilaginous joints. The development of new treatment neutralizing cytokines involved in the inflammatory attack has given relief and gives the promise of more effective treatment of already established disease. It is now time to set our eyes on a new vision to develop preventive and curative treatment based on knowledge of the unique and causative pathogenic mechanisms. To do this we believe it is important to identify the natural-selected polymorphisms that are associated with disease. These have proven to be extremely difficult to identify in complex diseases such as RA, but using animal models, this work is closer to reality. Animal models have recently been developed mimicking various aspects of the human disease. We will present an example in which a genetic polymorphism associated with the development of arthritis has been identified. On the basis of this finding, a new pathway involving control of immune tolerance by reactive oxidative species has been identified and a new class of anti inflammatory agents activating the induced oxidative burst protein complex is suggested.}},
author = {{Holmdahl, Rikard}},
booktitle = {{Immunotherapy in 2020 - Visions and Trends for Targeting Inflammatory Disease (Ernst Schering Foundation Symposium)}},
isbn = {{978-3-540-70850-6}},
issn = {{0947-6075}},
keywords = {{NADPH Oxidase: physiology; Reactive Oxygen Species; Chronic Disease; Rheumatoid: genetics; Arthritis; Animals; Rheumatoid: drug therapy; Animal; Disease Models; Genetic Predisposition to Disease; NADPH Oxidase: genetics; Humans; Major Histocompatibility Complex}},
language = {{eng}},
pages = {{1--15}},
publisher = {{Springer}},
title = {{Nature's choice of genes controlling chronic inflammation.}},
url = {{http://dx.doi.org/10.1007/2789_2007_036}},
doi = {{10.1007/2789_2007_036}},
volume = {{4}},
year = {{2007}},
}