Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

The understanding of the genetic basis of type 1 diabetes and other autoimmune diseases and the application of that knowledge to their treatment, cure and eventual prevention has been a difficult goal to reach. Cumulative progress in both mouse and human are finally giving way to some successes and significant insights have been made in the last few years. Investigators have identified key immune tolerance-associated phenotypes in convincingly reliable ways that are regulated by specific diabetes-associated chromosomal intervals. The combination of positional genetics and functional studies is a powerful approach to the identification of downstream molecular events that are causal in disease aetiology. In the case of type 1 diabetes, the availability of several animal models, especially the NOD mouse, has complemented the efforts to localize human genes causing diabetes and has shown that some of the same genes and pathways are associated with autoimmunity in both species. There is also growing evidence that the initiation or progression of many autoimmune diseases is likely to be influenced by some of the same genes.

Original publication

DOI

10.1002/047002139x.ch6

Type

Journal article

Journal

Novartis Foundation symposium

Publication Date

01/2005

Volume

267

Pages

57 - 65

Addresses

Juvenile Diabetes Research Foundation/Wellcome Trust Diabetes & Inflammation Laboratory, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Addenbrooke's Hospital, University of Cambridge, Cambridge CB2 2XY, UK.

Keywords

Animals, Mice, Inbred NOD, Humans, Mice, Diabetes Mellitus, Type 1, Genetic Predisposition to Disease, DNA, Antigens, Differentiation, Antigens, CD, Antigens, Differentiation, T-Lymphocyte, Base Sequence, Sequence Homology, Nucleic Acid, Polymorphism, Single Nucleotide, CTLA-4 Antigen, Inducible T-Cell Co-Stimulator Protein