Asset Details
Do you wish to reserve the book?
Genetics of Crohn disease, an archetypal inflammatory barrier disease
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Genetics of Crohn disease, an archetypal inflammatory barrier disease
Do you wish to request the book?
Genetics of Crohn disease, an archetypal inflammatory barrier disease
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Genetics of Crohn disease, an archetypal inflammatory barrier disease
2005
Overview
Key Points
The aetiology of Crohn disease, as an archetypal inflammatory barrier disease, involves inherited defects in several genes that maintain the integrity of barrier function.
CARD15
was identified as the first disease gene for Crohn disease; the main three variants identified all affect the ligand-binding domain of the NOD2 protein.
CARD15
variants confer an almost autosomal-recessive genetic effect that is much stronger than expected for a susceptibility gene in a polygenic condition.
Additional disease genes (
SLC22A4
,
SLC22A5
and
DLG5
) that have small odds ratios have been identified, but their involvement remains to be confirmed in independent samples.
The function of variability in susceptibility genes that leads to disease might be understood by studying evolutionary control.
Epidemiological trigger factors for inflammatory barrier diseases might interact with genetic susceptibility on the individual level through alterations of the human flora on body surfaces.
Chronic inflammatory disorders such as Crohn disease, atopic eczema, asthma and psoriasis are triggered by hitherto unknown environmental factors that function on the background of some polygenic susceptibility. Recent technological advances have allowed us to unravel the genetic aetiology of these and other complex diseases. Using Crohn disease as an example, we show how the discovery of susceptibility genes furthers our understanding of the underlying disease mechanisms and how it will, ultimately, give rise to new therapeutic developments. The long-term goal of such endeavours is to develop targeted prophylactic strategies. These will probably target the molecular interaction on the mucosal surface between the products of the genome and the microbial metagenome of a patient.
Publisher
Nature Publishing Group UK,Nature Publishing Group
