Published: 24 Jun 2021 992 views
Addison’s disease is a rare condition caused by autoimmune destruction of the adrenal glands. Untreated it is invariably fatal and following treatment it leaves people dependent on taking daily steroid medication, lifelong. Although knowledge is increasing, what causes most autoimmune diseases remains poorly defined at the molecular level. A defect in immune tolerance, whereby an abnormal immune system generates a destructive immune response against a ‘normal’ host protein has long been postulated and indeed, it has been confirmed that variants in several immune system genes contribute to Addison’s disease and other autoimmune conditions. Abnormalities or natural variations in the proteins that make up the target of the autoimmune response could also have a role in autoimmune diseases, and when these occur, they might be expected to correlate with the specific tissue or organ involved in the condition.
This studentship will explore the hypothesis that variation in steroid 21-hydroxylase, the key autoantigen for Addison’s disease, is a key reason that people develop the condition. The student will gain experience in a large variety of techniques including genotyping, gene expression analysis and tissue culture. Understanding the regulation of the key target proteins for the immune response in Addison’s disease will allow us to get important insights into why the condition develops and facilitate the development of new treatments for the condition.
| Application Deadline | 01 Jul 2021 |
| Type | PhD |
| Sponsor | Newcastle University |
| Gender | Men and Women |
100% of Home tuition fees paid and annual living expenses of £15,285 (full award).
You must have, or expect to achieve, at least a 2:1 Honours degree in genetics, immunology, biomedicine, biochemistry or a related area.
A further qualification such as an MSc or MRes is advantageous.
All applicants should complete the University’s postgraduate application system when applying for a studentship.
For more details, visit Newcastle University website.