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.

Project Overview:

The type 17/23 axis plays a key role in the pathogenesis of Ankylosing Spondylitis and realted human diseases including Psoriatic Arthritis, Psoriasis and Inflammatory Bowel Disease.  Understanding the immune pathogenesis of Type17 responses in AS has opened up opportunities for more effective targeted therapy. This project will take candidates from novel datasets (eg RNA seq) obtained from type 17 cells AS, and address their potential pathogenicity.

We have previously shown using in vitro assays with patient-derived cells that small molecule inhibitors of ERAP1, of the transcription factor ROR gamma T, of the (epigenetic) bromodomain readers and transcriptional co-activators CBP and p300 and of JAKs can all inhibit Type17 responses in vitro.

We will also luse established immunological assays to look for evidence of reciprocal regulation of regulatory T cell responses in SpA.


The Botnar Research Centre plays host to the University of Oxford's Institute of Musculoskeletal Sciences, which enables and encourages research and education into the causes of musculoskeletal disease and their treatment. Training will be provided in techniques including FACS and FACS analysis, cell culture, immunoassays, bacterial culture and metagenome analysis.

Relevant Publications: